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Effect of Schisandra chinensis Lignans on Neuronal Apoptosis and Mitochondrial Damage in Sleep Deprivation Model Rats #br# ZHAO Yi, LI Hua, HU Xia, CHANG Haixia Journal of Medical Molecular Biology    2025, 22 (5): 423-429.   DOI: 10.3870/j.issn.1672-8009.2025.05.002 Abstract （712）      PDF （5850KB）（46）       Knowledge map    Save Objective To explore the molecular mechanism by which Schisandra chinensis lignans (SCL) improve neuronal apoptosis and mitochondrial damage in the sleep deprivation (SD) model rats. Methods Forty-eight rats were divided into 6 groups: Control group, SD group, modafinil ( MOD) group ( positive control), and SCL treatment groups at different concentrations. The Morris water maze and Y-maze tests were used to assess the escape latency and behavioral accuracy of rats in each group, respectively. HE staining was used to detect hippocampal tissue pathological damage in rats, and TUNEL staining was used to detect cell apoptosis. JC-1 staining and ELISA were used to detect the levels of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) in rats’brain tissues and cells. An in vitro neuronal damage model was established using the ROS inducer 2, 3-dimethoxy-1, 4-naphthoquinone (DMNQ) to stimulate HT-22 cells. CCK-8 was used to measure cell viability. Western blotting was used to detect the expression levels of TLR4, MyD88, and p-NF-κB P65 in cells. Results Compared with those in the Control group, the escape latency of SD rats increased, and behavioral accuracy decreased. In contrast, rats treated with Mod or SCL showed reduced escape latency and increased behavioral accuracy (all P<0.05). Additionally, compared with rats in the Control group, rats in the SD group exhibited significant hippocampal tissue pathological damage, increased cell apoptosis, decreased MMP levels, and increased ROS levels. Mod or SCL intervention improved hippocampal tissue damage and cell apoptosis and reduced neuronal mitochondrial damage in SD rats (all P< 0. 05). Cellular experimental results showed that HT-22 cells in the DMNQ group had reduced viability, increased apoptosis, and increased mitochondrial damage and ROS levels when compared with those in the Control group. Mod or SCL treatment significantly improved the DMNQ-induced HT-22 cell damage. Moreover, compared with those in the Control group, the protein expression levels of TLR4, MyD88, and pNF-κB P65 in the DMNQ group cells were elevated, and Mod or SCL intervention significantly suppressed the levels of TLR4, MyD88, and p-NF-κB P65 in DMNQ-treated HT-22 cells. Conclusion SCL improves neuronal apoptosis and mitochondrial damage in SD rats by inhibiting the activation of the TLR4-MyD88-NF-κB pathway. Related Articles | Metrics

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Pancreatic Ductal Infusion of gRNA Carried by Adeno-Associated Viruses for β-Cell Adra2a Gene Editing #br# #br# ZHANG Xin, WANG Xinxin, LYU Tingting, HAN Xiao, ZHU Yunxia Journal of Medical Molecular Biology    2025, 22 (4): 305-310.   DOI: 10.3870/j.issn.1672-8009.2025.04.001 Abstract （328）      PDF （6060KB）（116）       Knowledge map    Save Objective This study aims to utilize the CRISPR / Cas9 system to achieve β-cell specific gene knockout in the pancreas through adeno-associated virus ( AAV8 ) carrying guide RNA ( gRNA ) targeting the Adra2a gene. Methods  RIP2 ( rat insulin Ⅱ promoter ) -Cre; Cas9KI / + mice were used to achieve β-cell-specific gene editing. In this model, the RIP2 promoter drives Cre recombinase expression selectively in pancreatic β cells, resulting in targeted activation of Cas9 in these cells. To enable efficient editing of the Adra2a gene, adeno-associated virus serotype 8, a low-immunogenic vector, was used to deliver gene-specific guide RNAs. AAV8 particles carrying gRNAs targeting Adra2a were injected via the pancreatic duct, enabling precise geneknockout in β cells. Results   Successful β-cell-specific gene knockout was achieved in the pancreas, confirmed by tissue analysis, PCR, and protein expression analysis. GFP expression was observed in the pancreas, and the targeted gene was successfully disrupted in β cells. Conclusion  The use of AAV carrying gRNA in the RIP2-Cre; Cas9KI / + mouse model provides an effective method for β-cell-specific gene knockout, offering a valuable tool for future studies of islet gene function. Related Articles | Metrics

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Identification and Validation of Pathogenic Variants in FBN1 Gene for 7 Patients with Marfan Syndrome #br# #br# GUO Chen#, MAO Tiantian#, NA Heya, XU Hongen, TIAN Yongan, ZHOU Yuyang, CHANG Xin, LIU Danhua, GAO Chengshan Journal of Medical Molecular Biology    2025, 22 (4): 311-318.   DOI: 10.3870/j.issn.1672-8009.2025.04.002 Abstract （249）      PDF （4852KB）（113）       Knowledge map    Save Objective Seven patients with Marfan syndrome (MFS) were screened for pathogenic variants in the fibrinogen-1 (FBN1) gene to explore the relationship between MFS and FBN1 gene mutations. Methods Genomic DNA was extracted from the peripheral blood of 7 patients andthen subjected to whole-exome sequencing. The candidate variants were validated, and their pathogenicity was interpreted. Results FBN1 (NM_ 000138. 5) gene variants were found in all sevenpatients, including 5 previously reported variants [ c. 367T > C ( p. Cys123Arg), c. 2093C > T(p. Pro698Leu), c. 7532 G > A (p. Cys2511Tyr), c. 6815 A > G (p. Tyr2272Cys), (c. 7279T > C(p. Cys2427Arg)], 1 novel variant [ c. 316C > T ( p. Gln106Ter)], and 1 first reported variant in Chinese [c. 6354C> T (p. Ile2118 = )] . According to the ACMG guidelines, six variants of above were classified as pathogenic / likely pathogenic, and one variant was classified as a variant of uncertain significance. Conclusion The identification of novel pathogenic variants in the FBN1 gene expands the known mutational spectrum and provides insights into the genetic basis of MFS, which is crucial for clinical diagnosis and patient management. Related Articles | Metrics

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Research Progress of Ferroptosis of Vascular Endothelial Cells in Atherosclerosis #br# ZHI Huimin, LI Yuanping, GAO Fen Journal of Medical Molecular Biology    2025, 22 (3): 295-299.   DOI: 10.3870/j.issn.1672-8009.2025.03.014 Abstract （220）      PDF （2761KB）（252）       Knowledge map    Save Atherosclerosis is the main pathological basis for cerebral infarction, coronary arteryatherosclerotic heart disease and other cardiovascular and cerebrovascular diseases. The abnormal death and functional disorder of vascular endothelial cells play an important role in it. Ferroptosis is a novel type of programmed cell death discovered in 2012, and there have been many studies showing that it plays an important role in the functional disorder and abnormal death of endothelial cells leading to AS. This review summarizes the mechanisms of ferroptosis and the possible mechanisms by which vascular endothelial cell ferroptosis leads to AS, and the drugs that may affect endothelial cell ferroptosis, providing a theoretical basis and research direction for the prevention and treatment of AS in clinical practice. Related Articles | Metrics

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Multi-omics Analysis and Validation of a Mouse Model of Diabetes Mellitus with Behavioral Abnormalities Based on High-throughput Mass Spectrometry #br# YANG Shufang, ZHANG Haoqiang, CHEN Xi, FAN Lin, YU Yefan, WANG Shaohua Journal of Medical Molecular Biology    2025, 22 (2): 131-138.   DOI: 10.3870/j.issn.1672-8009.2025.02.005 Abstract （214）      PDF （4692KB）（109）       Knowledge map    Save Objective To screen and verify the differentially expressed protein and the metabolites in a mouse model of type 2 diabetes mellitus with cognitive behavior abnormalities by highthroughput mass spectrometry. Methods High-throughput mass spectrometry was used to detect thelevels of hippocampal tissue protein expression and serum metabolites in the DB group ( abnormal cognitive behavior group) and the M group (normal cognitive behavior group). Target proteins and metabolites were screened out by bioinformatics and were then verified through Western blotting andELISA. Results ① 45 proteins and 119 positive ion-and 110 negative ion-metabolites were found tobe significantly expressed, and KEGG analysis showed that the differentially expressed genes were enriched in multiple metabolic pathways. ② Correlation analysis showed that serotonin-containing synapses and purine metabolism pathways were pathways co-enriched by multi-omics analysis. ③ pyruvate kinase L / R ( PKLR )、 arachidonic acid ( AA ) and adenosine 5′-monophosphate, (AMP) were differentially expressed. Conclusion PKLR, AA and AMP may be used as potentialbiomarkers for the diagnosis of type 2 diabetes mellitus with cognitive dysfunction. Related Articles | Metrics

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Effect of Linc279227 on Renal Injury in Diabetes Nephropathy Mice via PINK1 / Parkin Mediated Mitochondrial Autophagy #br# SHEN Qun, WANG Limin, DENG Wei, XIONG Wen, XIE Hongwu Journal of Medical Molecular Biology    2025, 22 (4): 319-324.   DOI: 10.3870/j.issn.1672-8009.2025.04.003 Abstract （198）      PDF （2780KB）（33）       Knowledge map    Save Objective To explore the effect and mechanism of TONCS _ 00279227(Linc279227) on renal injury in diabetes nephropathy mice. Methods Mice were divided into aControl group and a Model group. After successful modeling of db / db mice in the Model group, the mice kidney tissues were taken. qRT-PCR was used to detect the expression levels of Linc279227, PINK1, and Parkin in mice kidney tissues. Western blotting was used to detect the protein expression levels of LC3-Ⅱ , P62, PINK1, and Parkin in mice kidney tissues. Mouse renal podocyte MPC5 cells were divided into 3 groups: Vector group, Linc27922 group, and Linc27922 group. CCK8 and flow cytometry were used to detect cell proliferation and apoptosis. Western blotting was used to detect the expression levels of LC3-Ⅱ , P62, PINK1, and Parkin proteins in eachgroup of cells. Results Compared with those in the Control group, the expression levels of Linc279227 and P62 protein in the renal tissues of the model group mice were significantly upregulated (P< 0. 01), while the expression levels of PINK1 and Parkin mRNA and proteins and the LC3-Ⅱ protein were significantly downregulated (P < 0. 01) . Compared with those in the Vectorgroup, the mRNA and protein expression levels of PINK1 and Parkin and the protein expression level of LC3-Ⅱ in MPC5 cells of the Linc279227 group were significantly downregulated (P < 0. 01), and the expression level of P62 was significantly upregulated (P < 0. 01) . Compared with those inthe Linc279227 group, the LC3-Ⅱ expression level of MPC5 cells in the Linc27922 + FCCP group wasupregulated (P < 0. 01), the expression level of P62 was significantly downregulated (P < 0. 01), the cell proliferation ability was significantly increased (P<0. 05), and the cell apoptosis was significantly reduced (P < 0. 01) . Conclusion Linc279227 can mediate mitochondrial autophagy of nephropodocytes by regulating the PINK1 / Parkin pathway to affect renal injury in diabetes nephropathy mice. Related Articles | Metrics

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Effect of LINC00365 on Proliferation, Apoptosis, Migration, and Invasion of Thyroid Cancer Cells by Targeting miR-519d #br# Wufuer Yimaer, WANG Huguo, Daerhan Sailikebieke, DENG Chao, MaYire Nuermaimaiti Journal of Medical Molecular Biology    2025, 22 (2): 117-123.   DOI: 10.3870/j.issn.1672-8009.2025.02.003 Abstract （190）      PDF （4029KB）（174）       Knowledge map    Save Objective To investigate the effects and mechanisms of LINC00365 on proliferation, apoptosis, migration and invasion of thyroid cancer cells. Methods qRT-PCR was used todetect the relative expression level of LINC00365 in thyroid cancer tissues and thyroid cancer celllines. Thyroid cancer cells BHP-10-3 were divided into 5 groups: siNC group, si-LINC00365 group, si-LINC00365 + NC inhibitor group, si-LINC00365 + miR-519d inhibitor group, and blank group. Dual luciferase reporter gene experiment was used to detect the targeting relationship between LINC00365 and miR-519d. Cell proliferation ability was detected by CCK8, cell migration abilitywas detected by wound healing assay, cell invasion ability was detected by transwell assay, apoptosis rate was detected by flow cytometry. Results The relative expression level of LINC00365 were significantly upregulated in thyroid cancer tissues and thyroid cancer cells. miR-519d is the target gene of LINC00365. the proliferation, migration, and invasion abilities of BHP-10-3 in the siLINC00365 group and the si-LINC00365 + NC inhibitor group were significantly reduced ( P <0. 05), and the cell apoptosis rate was significantly increased ( P < 0. 01) when compared withthose in the blank group. The proliferation, migration, and invasion abilities of BHP-10-3 in the siLINC00365 + miR-519d inhibitor group were significantly increased (P < 0. 05), and the cell apoptosis rate was significantly reduced (P < 0. 01) when compared with those in the si-LINC00365 group. Conclusion LINC00365 can target miR-519d to affect the proliferation, migration, invasion and apoptosis of thyroid cancer cells. Related Articles | Metrics

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Effect of Phillyrin on Streptozotocin-induced Diabetic Mice and Its Mechanism #br# MA Haiping, LI Hongling Journal of Medical Molecular Biology    2025, 22 (3): 290-294.   DOI: 10.3870/j.issn.1672-8009.2025.03.013 Abstract （189）      PDF （648KB）（114）       Knowledge map    Save Objective To explore the effect and mechanism of phillyrin on streptozotocin induced diabetic mouse model. Methods  A diabetic mouse Model was established and mice wererandomly divided into 6 groups: Control group, Model group, phillyrin low-dose group, phillyrin medium-dose group, phillyrin high-dose group, and metformin group. The blood glucose value was measured by a glucose meter. The glycosylated hemoglobin detector was used to detect glycosylated hemoglobin. The levels of serum urea nitrogen, creatinine, 24 h urine protein, and the levels of TC, TG, LDL-C, HDL-C, MDA, SOD and GSH-Px were detected by kits. The levels of TNF-α,IL-6, and IL-1β were detected by ELISA. Results Compared with those in the Control group, thelevels of serum urea nitrogen, creatinine and urine protein, the levels of TC, TG, LDL-C, thelevel of MDA content, and the levels of TNF-α, IL-6 and IL-1β were increased in the Modelgroup, while the level of HDL-C, and the levels of SOD and GSH-Px contents were decreased(P < 0. 05). Compared with those in the Model group, the levels of serum urea nitrogen, creatinineand urinary protein, the levels of TC, TG and LDL-C, the level of MDA content, and the levels of TNF-α, IL-6 and IL-1β were decreased in the phillyrin medium and high dose groups and metformin groups, while the level of HDL-C, and the levels of SOD and GSH-Px contents were increased.(P < 0. 05). Conclusion Phillyrin can protect streptozotocin-induced diabetic mice by regulation ofdyslipidemia, oxidative stress, and inflammation. Related Articles | Metrics

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Effect of Sodium Aescinate on Atherosclerosis and Antioxidant Activity in Hyperlipidemia Model Rats #br# WANG Xuezhi, HAO Yafeng, YUAN Tao, XU Zhenkun, GAO Shuxian Journal of Medical Molecular Biology    2025, 22 (2): 187-193.   DOI: 10.3870/j.issn.1672-8009.2025.02.013 Abstract （182）      PDF （2015KB）（30）       Knowledge map    Save Objective To investigate the effect of sodium aescinate on atherosclerosis and antioxidant activity in hyperlipidemia model rats and its mechanism. Methods Seventy-two SD ratswere randomly divided into 6 groups: control group, model group, sodium aescinate 0. 5 mg / kg group、 1 mg / kg、 2 mg / kg groups and atorvastatin calcium 10 mg / kg group. Except for the control group, hyperlipidemia rat model was established in the other five groups. After the corresponding drug treatments were administered to each group, the rats were sacrificed, and myocardial tissue sections were prepared for HE staining. The blood lipids, whole blood viscosity indicators, and oxidative stress indicators were detected by automatic biochemical analyzer, and the atherosclerosis index (AI) and index of HDL-C / TC were calculated. The expression of Keap1-Nrf2 / ARE signalingpathway related proteins in rats were detected by using Western blotting. Results The myocardialfiber arrangement in the sodium aescinate 1 mg / kg and 2 mg / kg groups and the atorvastatin calcium10 mg / kg group were more dispersed than that in the model group, the degree of nuclear lysis anddamage were improved, the levels of TC, TG and LDL-C were decreased, the level of HDL-C wasincreased, the final body weight and AI were decreased, and the value of HDL-C / TC was increased when compared with those in the model group. The whole blood viscosity and the plasma viscosity were decreased, the level of ApoA-I and SOD and GSH-Px were increased, the level ofApoB100 and MDA was decreased, and the protein expression levels of Keap1, NQO1, ARE andp-Nrf-2 / Nrf-2 were significantly increased (P < 0. 05). Conclusion Sodium aescinate can improvemyocardial histopathological injury, regulate dyslipidemia, resist atherosclerosis and inhibit oxidative stress in hyperlipidemia model rats, and its mechanism may be related to the activation of Keap1-Nrf2 / ARE signaling pathway. Related Articles | Metrics

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Wutou Decoction Inhibits Inflammation and Oxidative Stress Induced Injury of Human Urogenic Stem Cells by Ahr/ LOC101928120 / SHC1 Signaling Pathway #br# WU Dan, TONG Liangming, LI Xi, ZHOU Ping, LI Jiefang Journal of Medical Molecular Biology    2025, 22 (3): 252-258.   DOI: 10.3870/j.issn.1672-8009.2025.03.007 Abstract （178）      PDF （2239KB）（69）       Knowledge map    Save Objective To investigate the mechanism by which Wutou decoction ( WTD) inhibits inflammatory and oxidative stress induced injury of human urogenic stem cells ( UdSC) bymodulating the aryl hydrocarbon receptor ( Ahr ) / long non-coding RNA ( LncRNA )LOC101928120 / SHC articulin 1 ( SHC1) signaling pathway. Methods UdSC cells were dividedinto 5 groups Control group, IL-1β group, IL-1β + WTD group, H2 O2 group, and H2 O2 + WTD group. CellTiterGlo assay and flow cytometry were applied to detect the proliferation and apoptosis in the cells of each group. qRT-PCR was applied to detect the expression levels of Ahr, LOC101928120, and SHC1 mRNA. Western blotting was applied to detect the expression levels of Ahr, HDAC1, SHC1, COL2, and SOX-9. ELISA was applied to detect the levels of IL-6, TNF-α, and MMP-13 in inflammation-induced UdSC cells. DCFH-DA fluorescent probe was applied todetect the ROS level in oxidative stress-induced UdSC cells. Results The A 560 nmvalue, the expression levels of Ahr mRNA and protein, LOC101928120, COL2, SOX-9 protein in the IL-1β group were lower than those in the Control group, and the values of above indexes in the IL-1β + WTDgroup were higher than those in the IL-1β group (P< 0. 05). The apoptosis rate, the levels of IL-6,TNF-α, MMP-13, and the expression levels of SHC1 mRNA and protein and HDAC1 protein in the IL-1β group were higher than those in the control group, and the values of above indexes in the IL-1β + WTD group were lower than those in the IL-1β group (P < 0. 05). TheA560 nm value, the expression levels of Ahr mRNA and protein, LOC101928120, COL2 and SOX-9 proteins in the H2O2 group were lower than those in the Control group, and the values of above indexes in the H2 O2 + WTD group were higher than those in the H2O2 group (P< 0. 05). The apoptosis rate, the proportion of ROS-positive cells, and the expression levels of SHC1 mRNA and protein and HDAC1 protein were higher than those in the Control group, and the above values in the H2 O2 + WTD groupwere lower than those in H 2O2 group (P< 0. 05). Conclusion WTD inhibits inflammatory and oxidative stress-induced injury in human UdSC, the mechanism may be achieved by modulating the Ahr / LOC101928120 / SHC1 signaling pathway. Related Articles | Metrics

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Research Progress of Intestinal Macrophages in Pathogenesis of Inflammatory Bowel Disease #br# BO Jiajia, GUO Tingting, SHEN Huiqin Journal of Medical Molecular Biology    2025, 22 (2): 205-210.   DOI: 10.3870/j.issn.1672-8009.2025.02.016 Abstract （173）      PDF （708KB）（144）       Knowledge map    Save Inflammatory bowel disease ( IBD) is a class of chronic recurrent gastrointestinalinflammatory diseases caused by inflammation and immune system disorders. Its pathogenesis is complex, and the immune system attacks the lining of the intestine, causing chronic inflammation and tissue damage. As a typical inflammatory disease, multiple immune cell types are involved in the pathogenesis of IBD. Among them, macrophages are thought to play a pivotal role. Intestinal macrophages are an important part of maintaining intestinal immune homeostasis and inhibiting the inflammatory response, which is of great significance for the treatment of inflammatory bowel disease. Given that macrophages can coordinate inflammation resolution and tissue repair, they are currently considered an attractive target for developing new treatments for inflammatory bowel disease. This review summarizes the research progress of immunomodulatory role of intestinal macrophages in IBD, so as to provide reference for the research of pathogenesis and the clinical treatment of IBD. Related Articles | Metrics

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Liensinine Induces Apoptosis in Glioma U251 Cells through ROS / JNK Pathway #br# LI Chengke, HE Qin, LUO Xiaoquan, FENG Hao, QIAO Fei Journal of Medical Molecular Biology    2025, 22 (2): 124-130.   DOI: 10.3870/j.issn.1672-8009.2025.02.004 Abstract （168）      PDF （5011KB）（412）       Knowledge map    Save Objective To investigate the effect of liensinine (LI) on apoptosis of U251 gliomacells and its mechanisms. Methods U251 and HEB cells were treated with different concentrationsof LI for 24 / 48 h, CCK8 assay and colony formation assay were performed to detect cell viability, flow cytometer was performed to detect apoptosis, and the expression levels of apoptotic proteins (Bax / Bcl-2, cleaved PARP) were detected by Western blotting. Cells were divided into 6 groups: control, LI, NAC, LI + NAC, SP600125, LI + SP600125. ROS was detected by DCFH-DA and p-JNK / cleaved PARP by Western blotting. U251 xenograft model was established to evaluate theeffect of LI on tumor volume / weight and tumor cell apoptosis. Results LI significantly inhibited theproliferation of U251 cells, decreased the colony formation of U251 cells, and promoted apoptosis. LI (80 μmol / L) induced ROS production and JNK phosphorylation, which were reversed byNAC and SP600125. In vivo experiments showed that LI inhibited tumor growth, reduced Ki67 positive cells, and promoted apoptosis. Conclusion LI selectively inhibits U251 via ROS / JNK-mediated apoptosis, demonstrating therapeutic potential for glioma. Related Articles | Metrics

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Effect of Nrf2 on Brain Injury and Microglial Cell Polarization in Neonatal Hypoxic-ischemic Encephalopathy Rats #br# WU Zhishan, XIAO Pei, LI Yanliang, YU Zhanzhang Journal of Medical Molecular Biology    2025, 22 (3): 229-236.   DOI: 10.3870/j.issn.1672-8009.2025.03.004 Abstract （167）      PDF （8862KB）（51）       Knowledge map    Save Objective To investigate the effect of nuclear factor E2-associated factor 2 (Nrf2)on brain injury in neonatal hypoxic-ischemic encephalopathy ( HIE) rats. Methods The experiments were divided into 4 groupd: Sham group, HIE group, Sham + Nrf2 group, and HIE + Nrf2group, with 10 neonatal SD rats in each group. The HIE model was established, and unloaded adenovirus or adenovirus containing Nrf2 overexpression vector was transfused into the ventricle. After 14days, cerebral infarction was detected by 2, 3, 5 triphenyltetrazolium chloride ( TTC) staining, and brain histopathological changes were observed by Hematoxylin-eosin (HE) staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β ( IL-1β), interleukin-6 (IL-6), and interleukin-10 ( IL-10 ) in brain tissues were determined by enzyme-linked immunosorbent assay (ELISA). The proportion of M1-type microglia labeled with ionized calcium binding adaptor molecule-1 (Iba-1) / inducible nitric oxide synthetase (iNOS) and the proportion of M2-type microglia labeled with Iba-1 / arginase 1 ( Arg-1) were detected by double-labeling immunofluorescence staining. The protein expression levels of iNOS, CD86, Arg-1, Macrophage mannose receptor(CD206), Nrf2, brain-derived neurotrophic factor (BDNF), and glia-derived neurotrophic factor(GDNF) were detected by Western blotting. Results Compared with those in the HIE group, thevolume of cerebral infarction in the HIE + Nrf2 group was significantly decreased, neuronal nucleus shrinkage was decreased, the levels of TNF-α, IL-1β and IL-6 in brain tissues were significantly decreased, and the levels of IL-10 were significantly increased, the proportion of Iba-1 + / iNOS + M1- type microglia was significantly decreased, and the proportion of Iba-1 + / Arg-1 + M2-type microglia was significantly increased, the expression levels of iNOS and CD86 protein in brain tissues were significantly down-regulated, the expression levels of Arg-1, CD206, Nrf2, BDNF and GDNF were significantly up-regulated (P < 0. 05). Conclusion Nrf2 can reduce neuroinflammation by promotingthe transformation of microglia from M1 type to M2 type to improve the brain injury of neonatal rats with HIE. Related Articles | Metrics

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CircITCH Regulates Proliferation and Invasion of Colorectal Cancer Cells via Targeting miR-106b #br# JIANG Linyan, SHEN Xiaowen, XU Meirong Journal of Medical Molecular Biology    2025, 22 (3): 223-228.   DOI: 10.3870/j.issn.1672-8009.2025.03.003 Abstract （161）      PDF （2758KB）（301）       Knowledge map    Save Objective To study the effect of circITCH on the proliferation, invasion of colorectal cancer cells via targeting miR-106b. Methods Colorectal cancer cell lines SW620, HT-29,HCT116, Caco-2, SW480, and normal colon epithelial cell line NCM460 were cultured. The expression levels of circITCH and miR-106b were detected, and HT-29 cells were selected for further experiments and were divided into 7 groups: Negative control ( NC) group, circITCH group, miR-NC group, miR-106b group, NC plasmid + miR-NC group, circITCH + miR-NC group, andcircITCH + miR-106b group. The A450 value, number of invasion cells and the expression levels of PTEN and B cell translocation gene 3 (BTG3) were detected. Results The expression level of circITCH in the SW620, HT-29, HCT116, Caco-2 and SW480 cells was lower than that in theNCM460 cell, while the expression level of miR-106b was higher in the NCM460 cell (P < 0. 05).Dual-luciferase reporter gene assay showed that miR-106b could bind with circITCH reporter gene). The expression levels of circITCH, PTEN, BTG3 in the circITCH group were higher than those inthe NC group, the expression level of miR-106b, A450 value, and the number of invasion cells were lower than those in the NC group (P < 0. 05). The expression level of miR-106b, A450 value, andthe number of invasion cells in the circITCH + miR-106b group were higher than those in the circITCH + miR-NC group, the expression levels of PTEN, BTG3 were lower than those in the circITCH + miR-NC group (P< 0. 05). Conclusion CircITCH can inhibit the proliferation and invasion of colorectal cancer cells via targeting miR-106b. Related Articles | Metrics

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In Vitro Study of miR-490-5p Regulating Inflammation and Angiogenesis in Hypoxy-induced Laryngeal Carcinoma FaDu Cells #br# TAN Yuanyuan, Aihemaitijiang Ailijiang, ZHOU Huiyin Journal of Medical Molecular Biology    2025, 22 (2): 101-107.   DOI: 10.3870/j.issn.1672-8009.2025.02.001 Abstract （156）      PDF （2251KB）（182）       Knowledge map    Save Objective To investigate the effect and molecular mechanism of microRNA-490-5p(miR-490-5p) on inflammatory response and angiogenesis in human laryngeal cancer cells inducedby hypoxia. Methods The human hypopharyngeal squamous cell carcinoma cell line FaDu was divided into 4 groups: control group (cultured in normoxic environment), hypoxic group (cultured in hypoxic environment), hypoxic + NC group (cultured in hypoxic environment and then transfected with mimics NC), and hypoxic + miR-490-5p group (cultured in hypoxic environment and then transfected with miR-490-5p mimics). The expression level of miR-490-5p in cells was detected by RT-qPCR, the cell proliferation activity was detected by CCK-8 method, the levels of tumor necrosis factor-α (TNF-α), interleukin (IL) -1β and IL-6 in the cell supernatant were determined by ELISA, the expression levels of proteins related to the nuclear factor κB (NF-κB) pathway in cellswas detected by Western blotting, the number of HUVEC tubes formed was detected by in vitro angiogenesis assay, the expression levels of vascular endothelial growth factor ( VEGF), epidermalgrowth factor ( EGF) and hypoxia-inducible factor-1α ( HIF-1α) in cells was detected by RTqPCR and Western blotting. Results Compared with those in the control group, the relative expression level of miR-490-5p in the hypoxia group was down-regulated (P < 0. 05), the proliferative activity was increased (P< 0. 05), the levels of TNF-α, IL-1β and IL-6 in supernatant were increased ( P < 0. 05 ), the relative expression levels of phosphorylated NF-κB P65 ( p-NF-κB P65) and phosphorylated IκB kinase α (p-IκBα) were up-regulated (P < 0. 05), and the number of HUVEC tubes was increased (P< 0. 05), the mRNA and protein relative expression levels of VEGF, EGF and HIF-1α were up-regulated (P< 0. 05). Compared with those in the hypoxia + NCgroup, the relative expression level of miR-490-5p in the hypoxia + miR-490-5p group was up-regulated (P< 0. 05), the proliferation activity was decreased (P < 0. 05), and the levels of TNF-α, IL-1β and IL-6 in supernatant were decreased (P< 0. 05), the relative expression levels of p-NF-κB P65 and p-IκBα were down-regulated, while the number of HUVEC tube formation was decreased (P< 0. 05 ), and the mRNA and protein expression levels of VEGF, EGF and HIF-1α were also down-regulated (P< 0. 05). Conclusion  Under hypoxic conditions, overexpression of miR-490-5p can inhibit the inflammatory response of laryngeal cancer cells and reduce the formation of tumor blood vessels. Related Articles | Metrics

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miR-24 Acts as Spongy of S100A8 in Kidney Tubular Epithelium Exosomes to Enhance Mitochondrial Damage and Promote Kidney Stone Disease #br# Diyaer Dilimulati, BAI Junbo, LIU Kaifang, Nafeisa Tuerdi, LI Jia Journal of Medical Molecular Biology    2025, 22 (2): 139-145.   DOI: 10.3870/j.issn.1672-8009.2025.02.006 Abstract （152）      PDF （1403KB）（828）       Knowledge map    Save Objective To investigate theeffect of miR-24 and S100A8 in exosomes of an in vitro kidney stone cell model on kidney stone disease and the underlying mechanism. Methods Human proximal tubular epithelial HKC-8 cells were used to establish a kidney stone cell model in vitro. HKC-8 cells were divided into four groups: the control group, the model group, the miR-24mimic + model group (miR-24 mimic was transfected into the cells of the model group), and the mimic NC + model group (mimic NC was transfected into the cells of the model group). Bioinformatics analysis was performed to analyze the relationship of miR-24 and S100A8 3′-UTR by using TargetScan v7. 2. Dual luciferase reporter assay was used to verify the direct interactions between miR-24 and S100A8 3′-UTR. Exosomes were extracted. The levels of miR-24 in exosomes was determined by qPCR. Western blotting was used to determine the protein expression levels of CD9, CD63 and S100A8 in exosomes, and the protein expression levels of PINK1, Parkin and Cytochrome C (Cyt-C) in cells. The levels of inflammatory cytokines TNF-α, IL-1β and IL-6 in cell supernatants and malondialdehyde ( MDA) in cells were determined by ELISA. The levels of reactive oxygenspecies ( ROS) were determined by DCFH-DA fluorescent dye method. Results Dual luciferasereporter assays had proved a direct interactions between miR-24 and S100A8 3′-UTR. miR-24 wasdown-regulated and S100A8 was up-regulated in the exosomes of the Model group (P< 0. 05), the expression levels of mitophagy markers of PINK1, Parkin and Cytochrome C were up-regulated (P<0. 05), the intracellular ROS and MDA levels were up-regulated (P< 0. 05), TNF-α, IL-1β andIL-6 were up-regulated in cell supernatants in the Model group ( P < 0. 05) when compared withthose in the Control group. The above indexes were all partially reversed in the miR-24 mimic + Model group (P< 0. 05), while there had been no significant difference in the mimic NC + Model group(P > 0. 05) when compared with those in the Model group. Conclusion MiR-24 was down-regulated and as “spongy” of S100A8 in exosomes of kidney stone cell model to up-regulate S100A8 expression, enhance mitochondrial damage and promote kidney stone disease. Related Articles | Metrics

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Bioinformatics Analysis of DHCR7 in Colon Cancer and Its Functional Validation #br# BAI Xiaogang, #, WANG Yanfeng, #, LIU Yongcheng, JI Haitao, Δ, ZHANG Jing Journal of Medical Molecular Biology    2025, 22 (2): 108-116.   DOI: 10.3870/j.issn.1672-8009.2025.02.002 Abstract （149）      PDF （8475KB）（59）       Knowledge map    Save Objective To explore the effects and regulatory mechanisms of dehydrocholesterolreductase 7 ( DHCR7) on the proliferation, apoptosis, migration, and invasion ability of coloncancer (CC) cells. Methods Using bioinformatics methods to analyze the relationship betweenDHCR7 expression and immune infiltration, prognosis, and sensitivity to anti-tumor drugs in colon cancer. qRT-PCR, Western blotting, and IHC were used to detect the mRNA and protein expression levels of DHCR7. Effect of DHCR7 knock-down on cell proliferation, cell cycle and apoptosis, cell migration and invasion was determined by MTT and colony formation assay, flow cytometry, wound-healing and Transwell assay, respectively. The key signaling pathways regulated by DHCR7were screened out through gene enrichment analysis and validated by Western blotting. Results  Bioinformatics analysis shows that the high expression of DHCR7 in colon cancer tissues was associated with the N-stage, specific survival, progression free survival, tumor immune infiltration level, and drug sensitivity of colon cancer. DHCR7 expression was upregulated in colon cancer tissues and cell lines. Knockdown of DHCR7 expression inhibited the proliferation, migration, and invasion of HCT166 cells. Wnt signaling pathway was one of the key signaling pathways regulated by DHCR7 inCC, and knockdown of DHCR7 inhibited Wnt signaling pathway. Conclusion DHCR7 regulatesthe Wnt signaling pathway to promote EMT in colon cancer cells, thereby promoting proliferation, migration, and invasion of HCT116 cells. Related Articles | Metrics

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Effect of Olaparib on Survival, Epithelial-mesenchymal Transition, and Tumor Stem Cell-like Characteristics in Ovarian Cancer ES2 Cells #br# YE Jing, ZHAO Jinrong , LI Ping, HAN Ci, ZHANG Xin, CHENG Wei, TIAN Xiaoru Journal of Medical Molecular Biology    2025, 22 (3): 217-222.   DOI: 10.3870/j.issn.1672-8009.2025.03.002 Abstract （147）      PDF （4428KB）（109）       Knowledge map    Save Objective To explore the effect of olaparib on the survival, epithelial-mesenchymal transition ( EMT ) and tumor stem cell-like characteristics of ovarian cancer ES2cells. Methods Ovarian cancer ES2 cells were culturedin vitro, and they were divided into 5groups: control group, low-dose olaparib group, middle-dose olaparib group, high-dose olaparib group and doxorubicin 0. 5 μmol / L group. Cells proliferation, apoptosis, invasion and migration were detected by 5-ethynyl-2′-deoxyuridine ( EDU) staining, flow cytometry, Transwell assay, and wound healing assay, respectively. The epithelial-mesenchymal transition ( EMT) of cells was observed under light microscope, tumor stem cell-like characteristics were observed by tumor spheroid formation assay, and protein expression level was detected by Western blotting. Results Compared with those in the control group, the apoptosis rate of ES2 cells and the expression level of Ecadherin were significantly increased in the low-, middle-, high-dose olaparib group and doxorubicin 0. 5 μmol / L group ( P < 0. 05), the ratio of EDU staining positive cells, number of invasioncells per unit area, cell wound-healing rate, number of tumor spheroid, spheroid diameter, and the expression levels of nuclear antigen Ki67, Survivin, vascular endothelial growth factor(VEGF), N-cadherin, cluster of differentiation 44 (CD44) and aldehyde dehydrogenase 1 (ALDH1) were significantly decreased in the middle-and high-dose olaparib group and doxorubicin 0. 5μmol / L group (P< 0. 05). Conclusion Olaparib of over 30 mg / L can significantly inhibit proliferation, invasion, and migration of ovarian cancer ES2 cells, and promote their apoptosis, which may be through inhibition of Ki67 and regulation of EMT. Related Articles | Metrics

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Construction and Functional Validation of a Novel Biological Activity Detection System for BMP-2#br# FU Yueyang, #, XIA Zhiyi#, YANG Jianxun, WANG Biru, ZHENG RuiΔ, YAN BoΔ Journal of Medical Molecular Biology    2025, 22 (5): 415-422.   DOI: 10.3870/j.issn.1672-8009.2025.05.001 Abstract （138）      PDF （1342KB）（87）       Knowledge map    Save Objective To develope a novel BMP-2 bioactivity detection system based on a dual-luciferase reporter gene stably transfected cell line (C2C12BBDE) to address the issues of low sensitivity, time-consuming procedures in traditional alkaline phosphatase ( ALP) activity assays, and cumbersome operational workflows in real-time fluorescent quantitative polymerase chain reaction(qRT-PCR ) methods. Methods This system integrates a BMP-2 responsive promoter driving NanoLuc luciferase (NLuc) expression with constitutively expressed Firefly luciferase ( Fluc) as an internal control via lentiviral transduction. Potential promoter interference was mitigated through strategic design of an inverse transcription unit and PolyA sequence insertion. Results This novel system achieved a dynamic detection range of 0-30 ng / mL, matching the sensitivity of qRT-PCR while demonstrating a statistically significant improvement over the ALP assay. Furthermore, the assay cycle was markedly reduced to 16 hours, representing an efficiency enhancement exceeding 700 % relative to the ALP method. Critically, the workflow is streamlined, obviating the need for complex RNA extraction and reverse transcription steps inherent in qRT-PCR. Conclusion The successful establishment of this system not only furnishes a standardized, high-throughput tool for BMP-2 bioactivity assessment but also provides a modular, adaptable technical paradigm for the development of bioactivity assays for other growth factors. This advancement holds substantial translational potential, significantly contributing to the rational development and clinical implementation of bone regenerative therapeutics. Related Articles | Metrics

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Protective Effect of Dihydrolycorine on Rats with CVB3-induced Viral Myocarditis #br# BAI Hongmin, YANG Yongzhong, CHEN Shujie, YANG Chao, LIU Wei Journal of Medical Molecular Biology    2025, 22 (3): 211-216.   DOI: 10.3870/j.issn.1672-8009.2025.03.001 Abstract （133）      PDF （7677KB）（131）       Knowledge map    Save Objective To explore the influence and mechanism of dihydrolycorine ( DL) onrats with viral myocarditis (VMC) induced by Coxsackie B3 virus (CVB3). Methods A total of72 SD rats were randomized into 6 groups: blank control group, model group, 10 mg / kg DLgroup, 20 mg / kg DL group, 40 mg / kg DL group, and Shenmai injection group (200 mg / kg),with 12 rats in each group. The CVB3-induced VMC model was established and intervened for 7days. The levels of serum myocardial enzymes and the hemodynamic indexes were detected. HE staining was used to detect the myocardial tissue pathological damage. TUNEL was used to detect myocardial cell apoptosis. Western blotting was applied to detect the expression levels of apoptosis andendoplasmic reticulum stress-related proteins. Results Compared with those in the model group,the pathological damage of myocardial tissue was alleviated, and the levels of serum myoglobin(Mb), creatine kinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI), the myocardialapoptosis rate and the protein expression levels of BCL2-associated X protein (Bax), C / EBP homologous protein (CHOP), glucose-regulated protein 78 ( GRP78) and GRP94 were reduced inthe 20 and 40 mg / kg DL groups and the Shenmai injection group ( P < 0. 05). Moreover, the leftventricular pressure (LVP), the maximum change rate of left ventricular pressure rise and fall ( ±dp / dtmax), and the protein expression levels of B-cell lymphoma-2 ( Bcl-2) and the cleaved /caspase-3 ratio rose in the 20 and 40 mg / kg DL groups and the Shenmai injection group ( P <0. 05). Conclusion DL can relieve the VMC myocardial injury and improve the cardiac dysfunction, which may be related to the inhibition of endoplasmic reticulum stress-mediated apoptosis. Related Articles | Metrics