Journal of Medical Molecular Biology

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

2025, 22(2): 101-107. doi:10.3870/j.issn.1672-8009.2025.02.001

Abstract ( 20 )

PDF (2251KB) ( 17 )

Related Articles | Metrics

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.

Bioinformatics Analysis of DHCR7 in Colon Cancer and Its Functional Validation #br#

BAI Xiaogang, #, WANG Yanfeng, #, LIU Yongcheng, JI Haitao, Δ, ZHANG Jing

2025, 22(2): 108-116. doi:10.3870/j.issn.1672-8009.2025.02.002

Abstract ( 16 )

PDF (8475KB) ( 11 )

Related Articles | Metrics

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.

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

2025, 22(2): 117-123. doi:10.3870/j.issn.1672-8009.2025.02.003

Abstract ( 13 )

PDF (4029KB) ( 13 )

Related Articles | Metrics

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.

Liensinine Induces Apoptosis in Glioma U251 Cells through ROS / JNK Pathway #br#

LI Chengke, HE Qin, LUO Xiaoquan, FENG Hao, QIAO Fei

2025, 22(2): 124-130. doi:10.3870/j.issn.1672-8009.2025.02.004

Abstract ( 13 )

PDF (5011KB) ( 5 )

Related Articles | Metrics

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.

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

2025, 22(2): 131-138. doi:10.3870/j.issn.1672-8009.2025.02.005

Abstract ( 10 )

PDF (4692KB) ( 13 )

Related Articles | Metrics

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.

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

2025, 22(2): 139-145. doi:10.3870/j.issn.1672-8009.2025.02.006

Abstract ( 13 )

PDF (1403KB) ( 5 )

Related Articles | Metrics

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.

Stromal Cells through Macrophage-Mediated Pathways in the Pathogenesis of Endometriosis #br#

CAO Wenchao

2025, 22(2): 146-152. doi:10.3870/j.issn.1672-8009.2025.02.007

Abstract ( 7 )

PDF (4210KB) ( 8 )

Related Articles | Metrics

Objective To investigate the effect of halofuginone (HF) on proliferation and apoptosis of endometriotic stromal cells ( ESCs) in endometriosis ( EMs) by regulation of macrophage polarization through peroxisome proliferator-activated receptor gamma ( PPARG) -leukemiainhibitory factor ( LIF) axis. Methods Normal endometrial stromal cells ( NESCs) and ectopicendometrial stromal cells ( EESCs) were treated with different concentrations of HF. CCK8 assay was used to detect the cell proliferation activity, and TUNEL assay was used to detect the cell apoptosis. Bioinformatics analysis was performed to identify the intersection of targets of HF, EMs, and macrophage. A co-culture system of macrophages and EESCs was established, cells were then divided into 7 groups: M0 + EESCs group、 M2 + EESCs group、 M2 + EESCsHF group、 M0 + EESCs oe-PPARG group、 M0 + EESCssh-PPARG group、 M0 + EESCsoe-PPARG + oe-LIF group、 M0 + EESCsoe-PPARG + HF group. ELISA was used to detect the concentrations of M1 macrophage markers (iNOS, IL-6) and M2 macrophage markers (Arg-1, TGF-β) in the cell supernatant. CCK8 and TUNEL assay wereused to detect the proliferation and apoptosis of EESCs, respectively. Results HF had no significant effect on the proliferation activity of NESCs (F = 0. 195, P = 0. 959), but significantly inhibited the proliferation of EESCs and promoted cell apoptosis (P< 0. 05). The levels of iNOS and IL-6 in the M2 + EESCs group were decreased when compared with those in the M0 + EESCs group,while the levels of Arg-1 and TGF-β were increased. In addition, the proliferation activity of EESCswas increased and the apoptosis was decreased. HF intervention reversed the results above ( P <0. 05). PPARG was identified as a key target in this study through bioinformatics analysis and literature search. The levels of iNOS and IL-6 in the cell supernatant of the M0 + EESCsoe-PPARG group weredecreased, while the levels of Arg-1 and TGF-β were increased when compared with those in the M0 + EESCs group. The proliferation activity of EESCs were increased and apoptosis were decreased(P< 0. 05), while an opposite results were obtained in the M0 + EESCssh-PPARG group (P < 0. 05).Furthermore, upregulation of LIF expression or HF intervention in the M0 + EESCsoe-PPARG + oe-LIF andM0 + EESCsoe-PPARG + HF groups led to the increase of iNOS and IL-6 levels and proliferation activity ofEESCs, and the decrease of Arg-1 and TGF-β and apoptosis when compared with the M0 + EESCsoe-PPARGgroup (P < 0. 05). Conclusion HF inhibits M2 polarization of macrophages and inhibitsthe proliferation of EESCs while promoting cell apoptosis by regulating the PPARG-LIF signalingpathway.

Effect of EPB41 Mediated Fatty Acid Oxidation on Esophageal Cancer Cell Proliferation and Migration #br#

LIN Jinqiu, WANG Liang, LIU Shizhu

2025, 22(2): 153-159. doi:10.3870/j.issn.1672-8009.2025.02.008

Abstract ( 10 )

PDF (4439KB) ( 9 )

Related Articles | Metrics

Objective To investigate the effect of erythrocyte membrane protein band 4. 1(EPB41) on the malignant phenotype of esophageal cancer cells and explore the possible underlyingmechanisms based on fatty acid oxidation ( FAO) mediated by the Wnt / β-catenin signaling pathway. Methods KYSE30 cells and KYSE150 cells in logarithmic growth phase were divided into 5groups each. The mRNA and protein expression levels, cell proliferation and migration rate, ATPlevel, NADPH / NADP + ratio, reactive oxygen species ( ROS ) and GSH levels were detected. Results In KYSE30 cells, the number of cell clones, cell migration rate, ATP level, NADPH / NADP + ratio, ROS level, and protein expression levels of Wnt3a, β-catenin, and nuclear β- catenin in cells were significantly increased in the EPB41 siRNA group (P < 0. 05), and fatty acidoxidation inhibitor and Wnt pathway inhibitor could reverse the effect of EPB41. In KYSE150 cells, the number of clones, cell migration rate, ATP level, NADPH / NADP + ratio, ROS level, and the expression levels of Wnt3a, β-catenin, and nuclear β-catenin proteins were significantly reduced in the cells in the EPB41 overexpression group (P < 0. 05), and the effect of EPB41 could be reversed by the fatty acid oxidation inducer and the Wnt pathway activator. Conclusion EPB41 expression is down-regulated in esophageal cancer cells. EPB41 overexpression can inhibit the proliferation and migration of esophageal cancer cells by suppressing the FAO pathway, which may be achieved by modulating the Wnt / β-catenin signaling transduction.

Protective Effect of Interfering with Rho-associated Coil Formation Protein Kinase 1 Expression on Mice with Acute Lung Injury #br#

LI Yufang, YANG Nan, YU Xiaowei, WEI Zhiwei, ZUO Tianxin, ZOU Fang

2025, 22(2): 160-165. doi:10.3870/j.issn.1672-8009.2025.02.009

Abstract ( 8 )

PDF (3239KB) ( 8 )

Related Articles | Metrics

Objective To investigate the effect of interference with Rho-associated coil formingprotein kinase 1 on lung injury induced by lipopolysaccharide (LPS) in mice. Methods C57BL / 6mice were divided into 4 groups: healthy control group, model group, negative control group and ROCK1 interference group, 10 mice each group. Acute lung injury was induced with LPS (5 mg / kg, i. p. ). The expression level of ROCK1 was detected by RT-PCR and Western blotting. The pulmonary function detection system was used to detect the airway resistance, resting ventilation and lung volume in mice. HE staining was used to observe the pathological damage of lung tissues, and Masson staining was used to observe the pulmonary fibrosis. Western blotting was used to detect the protein expression levels of α-SMA, TGF-β1 and FN. TUNEL assay was used to detect the lung cellapoptosis. The levels of iNOS, IL-6 and TNF-α were detected by ELISA. Results ROCK1 washighly expressed in the model group and the lung injury was more serious when compared with thatin the healthy control group. ROCK1 interference group had lower expression level of ROCK1 (P <0. 05), and increased airway resistance, resting ventilation and lung volume when compared withthe model group (P < 0. 05). The pathological injury and degree of fibrosis in lung tissues were improved in the ROCK1 interference group, and the expression levels of α-SMA, TGF-β1 and FN proteins were significantly decreased (P< 0. 05). The number of apoptotic cells in lung tissues was significantly decreased (P< 0. 05), and the levels of iNOS, IL-6 and TNF-α in peripheral bloodwere significantly decreased in the ROCK1 interference group when compared with those in themodel group (P < 0. 05). Conclusion Interfering ROCK1 expression can improve lung function,pulmonary fibrosis, apoptosis and inflammation in LPS-induced acute lung injury mice.

Knockdown of lncRNA LINC01296 Inhibited Proliferation and Stemcell Characteristics of Osteosarcoma Cells through Wnt / β-catenin Pathway #br#

LIU Guangfei, GUO Zhiyuan, WANG Yanhua, LU Shouliang, GUO Lei, CHENG Cai

2025, 22(2): 166-172. doi:10.3870/j.issn.1672-8009.2025.02.010

Abstract ( 7 )

PDF (2960KB) ( 9 )

Related Articles | Metrics

Objective To investigate the effect of knocking down long non-coding RNA ( lncRNA) LINC01296 on the proliferation capacity and stem-cell characteristics of human osteosarcoma (OS) cells, and to explore the related mechanisms. Methods Human normal osteoblast cellline hFOB1. 19 and human OS cell lines MG63, U2OS and Saos2 were cultured, and the expression level of lncRNA LINC01296 was detected by qRT-PCR. MG63 cells were divided into 4 groups: control group, siRNA negative control group ( negative control siRNA was transfected into cells), LINC01296 siRNA interference group (LINC01296 siRNA was transfected into cells), LINC01296 siRNA + LiCl group ( LINC01296 siRNA was transfected into cells and cultured with 10 mmol / L Wnt / β-catenin pathway activator LiCl for 24 h). The expression level of lncRNA LINC01296 in each group was detected, the survival rate of cells in each group was detected by CCK-8 method, the proliferation of cells was observed by EdU staining, and the spheroid number in each group was detected by tumor cell spheroid formation assay, the expression levels of stem-cell related proteins (Nanog, OCT-4, SOX2) and Wnt / β-catenin pathway-related proteins (β-catenin, c-Myc, Cyclin D1) in cells of each group were detected by Western blotting. Results The relative expressionlevel of lncRNA LINC01296 in the human OS cell lines MG63, U2OS and Saos2 was significantlyhigher than that in the hFOB1. 19 cells (P< 0. 05). The survival rate, the proportion of EdU positive cells, and the number of tumor cell spheres of MG63 cells in the LINC01296 siRNA group wassignificantly decreased when compared with those in the control group (all P< 0. 05), in addition,the relative expression levels of Nanog, OCT-4, SOX2, β-catenin, c-Myc and Cyclin D1 in theLINC01296 siRNA group were significantly down-regulated (P< 0. 05). The survival rate, the proportion of EdU positive cells, and the number of tumor cell spheres of MG63 cells in theLINC01296 siRNA + LiCl group was significantly increased when compared with those in theLINC01296 siRNA group ( all P < 0. 05 ), at the same time, the relative expression levels ofNanog, OCT-4, SOX2, β-catenin, c-Myc and Cyclin D1 in the cells were significantly up-regulated (P< 0. 05). Conclusion Targeted knockout of lncRNA LINC01296 in OS cells can inhibit cellproliferation and reduce osteosarcoma cell stemness, which may be related to inhibiting the activation of Wnt / β-catenin pathway.

Diagnostic Value of miR-425-5p in Endometrial Cancer and Effect of Inhibiting miR-425-5p on Proliferation, Migration and Apoptosis in Endometrial Cancer Cells #br#

BAI Mihong, ZHANG Jie, KOU Li, WANG Jinbo

2025, 22(2): 173-179. doi:10.3870/j.issn.1672-8009.2025.02.011

Abstract ( 10 )

PDF (2963KB) ( 4 )

Related Articles | Metrics

Objective To analyze the diagnostic value of miR-425-5p in endometrial cancer(EC) and the effect of inhibiting miR-425-5p on the proliferation, migration, and apoptosis of ECcells. Methods The expression level of miR-425-5p in serum and tissues of patients with EC andbenign uterine lesions was detected by RT-qPCR, and was compared among patients with differentpathological characteristics of EC. The relationship between miR-425-5p expression in the tissues andserum and the pathological characteristics was analyzed, as well as its diagnostic value for EC. Theexpression level of miR-425-5p in normal endometrial epithelial hEEC cells, endometrial carcinomaIshikawa, HEC-1A, HEC-1B cells was detected by RT-qPCR. Ishikawa cells were divided into 3groups: Con group ( no treatment control), anti-miR-NC group ( transfected with anti-miR-425-5p) and anti-miR-425-5p group (transfected with anti-miR-425-5p). RT-qPCR was used to detect the miR-425-5p expression level. MTT and flow cytometry were used to detect cell proliferation, cell cycle and apoptosis. cell migration was detected by Transwell. The expression levels of CyclinD1,PCNA, Bax, Bcl-2 and MMP9 were detected by Western blotting. Results The expression level ofmiR-425-5p in serum and tissues of the endometrial carcinoma group was higher than that of the benign lesion group (P< 0. 05). There were statistically significant differences when comparing the expression level of miR-425-5p in patients with different lymph node metastasis statuses, FIGO stagesand degrees of differentiation (P< 0. 05). The expression of miR-425-5p in tissues and serum was positively correlated with FIGO stage, lymph node metastasis, and degree of differentiation ( r =0. 793, 0. 689, 0. 665, 0. 694, 0. 652, 0. 672, P < 0. 05). The AUC of miR-425-5p in tissuesand serum for the diagnosis of EC were 0. 782 and 0. 762, respectively. The sensitivities were74. 36 % , 71. 79 % , specificity, and the specificities were 71. 79 % , 70. 51 % , respectively. The expression level of miR-425-5p in endometrial carcinoma Ishikawa, HEC-1A, HEC-1Bcells was increased when compared with that in hEEC cells ( P < 0. 05). The expression level ofmiR-425-5p, cell activity, the proportion of cells in the S phase, the number of migrated cells,and the expression levels of Bcl-2, MMP9, CyclinD1 and PCNA proteins in the anti-miR-425-5pgroup were significantly decreased when compared with those in the anti-miR-NC group or the Congroup, while the proportion of cells in the G0 / G1 phase, the apoptosis rate and the protein expression of Bax were significantly increased (P < 0. 05). Conclusion miR-425-5p is highly expressedin EC tissues and serum, its expression level in EC tissues and serum is related to the patients’FIGO stage, lymph node metastasis and degree of differentiation. It has certain values in the diagnosisof EC. Moreover, inhibition of miR-425-5p can significantly inhibit the proliferation and migration ofEC cells, and induce cell apoptosis.

Oridonin Improves Myocardial Ischemia-reperfusion Injury by Attenuating Endoplasmic Reticulum Stress-induced Apoptosis #br#

YUAN Fang, SONG Haiping, WANG Congcong, HOU Binbin, HOU Aijun, ZHAO Weijin

2025, 22(2): 180-186. doi:10.3870/j.issn.1672-8009.2025.02.012

Abstract ( 12 )

PDF (4184KB) ( 4 )

Related Articles | Metrics

Objective To explore the effect of oridonin on myocardial ischemia-reperfusion injury. Methods A total of 108 rats were randomly divided into 6 groups: sham operation group, I /R group, low-dose, middle-dose and high-dose oridonin treatment groups (2. 5, 5 and 10 mg / kg, continuous intervention for 7 days before surgery) and positive control group (intravenous injection of alprostadil after modeling), with 18 rats in each group. The hemodynamic indicators, myocardial pathological injury, serum oxidative stress indicators, endoplasmic reticulum stress and apoptosisrelated mRNA and protein expression levels and the apoptosis of myocardial cells were detected. Results The oxidative stress indicator and hemodynamics were significantly improved in thehigh-dose oridonin treatment group and positive control group when compared with those in the I / Rgroup, and the myocardial infarction range and myocardial cell apoptosis rate were decreased (P <0. 05). The mRNA expression levels of endoplasmic reticulum stress-related genes were down-regulated (P < 0. 05), and the expression levels of apoptosis-related proteins were declined (P < 0. 05). Conclusion Oridonin can alleviate the myocardial injury in I / R rats, which may be related to alleviating oxidative stress injury and attenuating endoplasmic reticulum stress-induced apoptosis.

Effect of Sodium Aescinate on Atherosclerosis and Antioxidant Activity in Hyperlipidemia Model Rats #br#

WANG Xuezhi, HAO Yafeng, YUAN Tao, XU Zhenkun, GAO Shuxian

2025, 22(2): 187-193. doi:10.3870/j.issn.1672-8009.2025.02.013

Abstract ( 14 )

PDF (2015KB) ( 5 )

Related Articles | Metrics

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.

Application of miR-495-3p and Mn-SOD Gene Detection in Disease Evaluation of Diabetes Nephropathy Patients #br#

ZHU Shuang, HU Xiao

2025, 22(2): 194-199. doi:10.3870/j.issn.1672-8009.2025.02.014

Abstract ( 12 )

PDF (863KB) ( 3 )

Related Articles | Metrics

Objective To explore the application value of gene detection of miR-495-3p andmanganese superoxide dismutase (Mn-SOD) in the disease evaluation of diabetes nephropathy patients. Methods A total of 150 patients with diabetes nephropathy who were treated in HuangshiCentral Hospital from January 2022 to December 2023 were selected, and another 150 patients with diabetes and 150 healthy people were included in this study as controls. the differences of miR-495-3p expression and Mn-SOD genotypes in each group were compared, and the value of miR-495-3p expression and Mn-SOD genotypes in predicting poor prognosis of diabetes nephropathy were analyzed. Results The expression level of miR-495-3p in the group of diabetes nephropathy patients was (0. 56 ± 0. 14), which was significantly lower than that of diabetes and healthy people (P<0. 05). There was a statistically significant difference in the distribution of genotypes at the 9 and5 777 loci of Mn-SOD gene in diabetes nephropathy, diabetes and healthy people (P< 0. 05). Theproportion of CT + CC genotype at the 9 loci of Mn-SOD gene in diabetes nephropathy was 40. 00 % ,the proportion of CT + CC genotype at position 5 777 of the Mn-SOD gene was 98. 00 % . The expression level of miR-495-3p in diabetes nephropathy patients with T2DM duration ≥ 10 years was(0. 46 ± 0. 14), which was significantly lower than that in patients with T2DM duration < 10 years(P< 0. 05). The expression level of miR-495-3p in patients with poor prognosis of diabetes nephropathy was (0. 47 ± 0. 14), which was significantly lower than that in patients with good prognosis(P< 0. 05). The proportion of CT + CC at Mn-SOD gene locus 9 genotype in patients with poor prognosis was 73. 33 % , which was significantly higher than that in patients with good prognosis (P <0. 05). There was no significant difference in CT + CC ratio of Mn-SOD gene 5 777 genotype betweenpatients with poor prognosis and those with good prognosis ( P > 0. 05). The area under the ROCcurve for predicting poor prognosis of miR-495-3p and Mn-SOD gene 9 locus genotypes was 0. 784(95 % CI: 0. 705 - 0. 863) and 0. 786 (95 % CI: 0. 700 - 0. 872), respectively ( P < 0. 05).Conclusion The level of miR-495-3p in patients with diabetes nephropathy is reduced, miR-495-3p expression and Mn-SOD genetypes have certain application values in predicting the prognosis ofdiabetes nephropathy.

Signal Pathways Related to the Virulence of Aspergillus fumigatus under Stress Conditions #br#

GAO Liang, MA Yan

2025, 22(2): 200-204. doi:10.3870/j.issn.1672-8009.2025.02.015

Abstract ( 11 )

PDF (722KB) ( 20 )

Related Articles | Metrics

Aspergillus fumigatus (A. fumigatus) is a common opportunistic pathogen. Its sporesare abundant in the human environment and are the main cause of invasive aspergillosis, with highinfection rate and mortality rate. The ability of A. fumigatus to resist and adapt to adverse environments is closely related to their virulence and is the key to the treatment of A. fumigatus infection. This review introduces the signal transduction pathways, including the unfolded protein response pathway, high osmolarity glycerolpathway, cell wall integrity pathway and calcium-calcineurin pathway, in A. fumigatus under different stress conditions and their effects on the growth,virulence and resistance to antifungal drugs. It provides new ideas for the development of innovative drugs for the treatment of invasive aspergillosis.

Research Progress of Intestinal Macrophages in Pathogenesis of Inflammatory Bowel Disease #br#

BO Jiajia, GUO Tingting, SHEN Huiqin

2025, 22(2): 205-210. doi:10.3870/j.issn.1672-8009.2025.02.016

Abstract ( 11 )

PDF (708KB) ( 6 )

Related Articles | Metrics

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.