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31 January 2025, Volume 22 Issue 1
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P300 Inhibits Intervertebral Disc Degeneration through Nrf2 / HO-1 / NF-κB Signaling in Rat Scoliosis Model #br#
ZHAO Xianbin, GUO Shining, BO Wenting
2025, 22(1):  1-7.  doi:10.3870/j.issn.1672-8009.2025.01.001
Abstract ( 10 )   PDF (1364KB) ( 13 )  
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Objective To investigate the effect and potential regulatory mechanism of histoneacetyltransferase P300 on the degeneration of nucleus pulposus cells (NPCs) in the intervertebral discs in the rat scoliosis model. Methods NPCs were cultured and divided into 4 groups: the untreated control group, the interleukin-1β ( IL-1β) -induced degeneration group ( IL-1β group), the IL-1β combined with P300 treatment group (IL-1β + P300 group), and the P300 treatment alone group ( P300 group). Cell proliferation activity was detected using the Cell Counting Kit-8 (CCK-8) assay. The levels of TNF-α and IL-6 were measured using enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was determined using flow cytometry. The expression levels of sex determining region Y-box 9 ( SOX9 )、 collagen type Ⅱ ( COL-Ⅱ ), matrix metalloproteinase-13 (MMP-13), A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5), inhibitor of nuclear factor-kappa B-α ( IκBα), phosphorylated IκBα ( p-IκBα), phosphorylated NF-κB P65 (p-P65), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) in the cells were analyzed using Western blotting. Additionally, 40 adult specific pathogen-free (SPF) female SD rats were divided into 4 groups: sham surgery group, scoliosis model group, scoliosis model + P300 group, and scoliosis model + P300 + Nrf2-IN-3 group. The scoliosis model was established by removing the upper limbs and tail of the rats through surgery. In the scoliosis model + P300 group, P300 was intravenously injected [15 mg / (kg· d), 30 d] after modeling. In the scoliosis model + P300 + Nrf2-IN-3 group, P300 [15 mg / ( kg· d), 30 d] and the Nrf2 inhibitor Nrf2-IN-3 [23. 5 mg / ( kg · d), 30 d] were intravenously injected after modeling. After 30 days, the nucleus pulposus tissues from the T12-L1 intervertebral discs were collected, and the expression levels of SOX9, COL-Ⅱ , MMP-13, and ADAMTS-5 were determined usingWestern blotting. Results Compared with the control group, the IL-1β group showed decreasedcell viability, increased cell apoptosis, upregulated expression levels of TNF-α, IL-6, MMP-13, ADAMTS-5, p-P65, and p-IκBα, and downregulated expression levels of SOX9, COL-Ⅱ ,IκBα, Nrf2, and HO-1 (all P< 0. 05). Compared with the IL-1β group, the IL-1β + P300 groupshowed increased cell viability, decreased cell apoptosis, decreased expression levels of TNF-α, IL-6, MMP-13, ADAMTS-5, p-P65, and p-IκBα, and increased expression levels of SOX9,COL-Ⅱ , IκBα, Nrf2, and HO-1 ( all P < 0. 05). Compared with the sham surgery group, thescoliosis model group showed decreased expression levels of SOX9 and COL-Ⅱ , and increased expression levels of MMP-13 and ADAMTS-5 ( all P < 0. 05 ). Compared with the scoliosis modelgroup, the scoliosis model + P300 group showed increased expression levels of SOX9 and COL-Ⅱ ,and decreased expression levels of MMP-13 and ADAMTS-5 ( all P < 0. 05). Compared with thescoliosis model + P300 group, the scoliosis model + P300 + Nrf2-IN-3 group showed decreased expression levels of SOX9 and COL-Ⅱ , and increased expression levels of MMP-13 and ADAMTS-5(all P< 0. 05). Conclusion P300 inhibits intervertebral disc degeneration by regulating the Nrf2 /HO-1 / NF-κB signaling pathway in the rat scoliosis model.

Hydatid Antigen B Promote RANKL / NF-κB / TAK1-mediated Osteoclastogenesis via Inhibition of TAZ #br#
Wuluhan Mahan, XIE Zengru
2025, 22(1):  8-15.  doi:10.3870/j.issn.1672-8009.2025.01.002
Abstract ( 5 )   PDF (2352KB) ( 4 )  
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Objective To investigate the molecular mechanisms of hydatid antigen-B (Hyd-B) in osteoclastogenesis. Methods Cell experiment group-1: Bone marrow mesenchymal stem cells(BMSCs) were divided into 3 groups (Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group), cells in the MCSF + RANKL group and MCSF + RANKL + Hyd-B group were induced to differentiate into osteoclasts by using macrophage colony-stimulating factor (MCSF) combined with soluble receptor activator of nuclear factor-κb ligand (RANKL), and then treated with or without Hyd-B respectively. Cell experiment group-2: BMSCs were divided into Ctrl group and Hyd-B treatment group (Treat group), the effect of Hyd-B on the direct interaction between TAZ and TAK1 was determined by co-immunoprecipitation ( co-IP). IP was performed by using antiTAK1 antibody, and TAZ expression level was detected by IB. Cell experiment group-3: BMSCs were divided into 5 groups: Control group, MCSF + RANKL group, MCSF + RANKL + Hyd-B group, MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group. TAZ overexpression plasmid or vector plasmid was transfected to the BMSCs in the MCSF + RANKL + Hyd-B + TAZ-OE group and MCSF + RANKL + Hyd-B + OE-vector group respectively. qPCR was used to detect the mRNA expression levels of osteoclast differentiation markers of TRAP and Cathepsin K. Western blotting was used to detect the expression levels of nuclear p-P65, cytoplasmic P65, nuclear NFATc1, p-AKT, AKT, p-ERK 1 / 2, ERK 1 / 2, p-TAZ, TAZ and TAK1. Results Compared with those in the Control group, the TRAP and Cathepsin K mRNA expression levels in the MCSF + RANKL and MCSF + RANKL + Hyd-B groups were increased (P <0. 05); the expression levels of p-P65, p-AKT and p-ERK 1 / 2 were increased (P < 0. 05); theexpression levels of p-P65 and NFATc1 in nucleus were increased (P < 0. 05). The expression levels of the above indicators were further increased in the MCSF + RANKL + Hyd-B group when compared with those in the MCSF + RANKL group ( P < 0. 05). Compared with those in the MCSF +RANKL + Hyd-B group, the expression levels of the above indicators in MCSF + RANKL + Hyd-B +TAZ-OE group were all reduced (P < 0. 05). Co-IP results showed that Hyd-B treatment enhancedthe interaction between TAZ and TAK1 ( P < 0. 05). Compared with those in the Ctrl group, thephosphorylated level of cytoplasmic TAZ in Treat group was increased, the expression level of TAZwas reduced (P< 0. 05). Conclusion Hyd-B can promot the RANKL / NF-κB / TAK1-mediated osteoclastogenesis through inhibition of TAZ.

Effect of Lupeol on Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells by Targeting CDC25A #br#
ZHU Yexin, DENG Liping
2025, 22(1):  16-22.  doi:10.3870/j.issn.1672-8009.2025.01.003
Abstract ( 7 )   PDF (6492KB) ( 10 )  
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Objective To analyze the effect of lupeol on proliferation, migration, invasion of lung adenocarcinoma cells by targeting CDC25A. Methods The targets of lupeol and their correlation with clinical phenotypes of lung adenocarcinoma were analyzed by bioinformatics. A549 and Calu-3 cells were divided into 6 groups: control group, lupeol group, vector group, lupinol + vector group, silence group and lupinol + silence group. The cells activity, migration and invasion were detected. The xenograft models of nude mice with lung adenocarcinoma were constructed to observe the effects of lupeol on volume and weight of xenograft tumors, and expression levels of Ki67 and CDC25A proteins. The relationship between expression level of CDC25A protein and the concentration and time of lupeol treatment was measured. Results Bioinformatic analysis showed thatCDC25A might be one of lupeol targets, and the expression level of CDC25A was closely related tothe progression of lung adenocarcinoma. The survival rates and colony numbers of A549 and Calu-3cells were decreased with the increase of lupeol concentration (P < 0. 05). The number of migrationand invasion lung adenocarcinoma cells in the lupeol group were significantly lower than those in thecontrol group ( P < 0. 05), the volume and weight of xenograft tumors, the expression levels of Ki67 and CDC25A were significantly lower than those in the control group (P < 0. 05). The expression level of CDC25A was significantly decreased with the increase of time and concentration of lupeol treatment (P < 0. 05). The expression level of CDC25A, the cells activities, the number of colonies and migration and invasion cells in the lupinol + vector group, the silence group and the lupinol +silence group were significantly lower than those in the vector group (P < 0. 05). Conclusion Lupeol can inhibit malignancy of lung adenocarcinoma tumor cells by down-regulating CDC25A.

Mechanism of Schisantherin B Inhibiting Proliferation of Uterine Corpus Endometrial Carcinoma Cells and Epithelial-mesenchymal Transition by Targeting PTGS1 #br#
YE Jing, LI Ping, ZHAO Jinrong, HAN Ci, ZHANG Xin, XU Yuanyuan, SU Huiling
2025, 22(1):  23-28.  doi:10.3870/j.issn.1672-8009.2025.01.004
Abstract ( 5 )   PDF (5694KB) ( 6 )  
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Objective To analyze the mechanism of Schisantherin B inhibiting the proliferationof uterine corpus endometrial carcinoma ( UCEC ) cells and epithelial-mesenchymal transition( EMT ) by targeting prostaglandin-endoperoxide synthase 1 ( PTGS1 ) . Methods The target( PTGS1) of Schisantherin B was predicted by TargetNet. The relationship between the expression ofPTGS1 and the clinicopathological characteristics of UCEC was analyzed by TCGA database. Thecontrol group, Schisantherin B group and sh-PTGS1 group were set up. The survival and colony formation abilities of cells, and the expression levels of EMT associated proteins were detected. Theeffect of PTGS1 on volume and weight of xenograft tumors, and the level of proliferation index(Ki67) were observed. Ishikawa and HEC108 cell lines with stable overexpression of PTGS1 wereconstructed. The effect of Schisantherin B on survival, colony formation abilities, and expressionlevels of EMT proteins of Ishikawa and HEC108 cells with PTGS1 overexpression were detected. Results Compared with those in the control group, the proliferation and numbers of cell colonies, and the expression levels of PTGS1, Vimentin, N-cadherin and Snail in the sh-PTGS1 group and the Schisantherin B group were significantly decreased, the expression level of E-cadherin in the above two groups was significantly increased; the volume and weight of xenograft tumor tissues,and the expression level of Ki67 in the sh-PTGS1 group were significantly decreased ( P < 0. 05). However, the expression level of E-cadherin was significantly decreased in the PTGS1 overexpression group, the expression levels of PTGS1, Vimentin, N-cadherin, Snail, and the cell viabilities, and number of cell colonies of Ishikawa and HEC108 cells were significantly increased when compared with those in the control group (P< 0. 05). In addition, when compared with those in theSchisantherin B group, the expression level of E-cadherin was significantly decreased in the Schisandrin B + PTGS1 overexpression group, while the expression levels of PTGS1, Vimentin,N-cadherin, Snail were significantly increased (P < 0. 05). Conclusion Schisantherin B may inhibit the proliferation and EMT of UCEC cells by down-regulating PTGS1.

Jatrorrhizine Inhibit Progression of Osteosarcoma by Downregulation of MAOB #br#
LI Xiaowen, ZHAO Jie, JIANG Liqiang, ZHANG Kai, JIA Haidong, ZHANG Cun
2025, 22(1):  29-34.  doi:10.3870/j.issn.1672-8009.2025.01.005
Abstract ( 5 )   PDF (7427KB) ( 4 )  
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Objective To investigate the effect of jatrorrhizine on the development of osteosarcoma and its mechanism. Methods The targets of jatrorrhizine on osteosarcoma were screenedthrough network pharmacology analysis, and GSEA enrichment was used to analyze the relationshipbetween the expression level of monoamine oxidase B (MAOB) and the clinical phenotypes of osteosarcoma. The cell activities of osteosarcoma cells MG63 and U2OS were detected under differentdoses of jatrorrhizine (0, 2, 4, 8, 16 μmol / L), and the optimal jatrorrhizine dose for follow-upfunctional test was selected. CCK-8 method and Transwell assay were used to detect the cell proliferation, migration and invasion of MG63 and U2OS, and Western blotting was applied to detect theprotein expression levels of cell proliferation-associated antigen Ki67, matrix metalloproteinase 2(MMP2) and MMP9. The subcutaneous transplant models of osteosarcoma in nude mice were established, and the weight and volume of tumor tissues of each group were measured, and the expression level of Ki67 was determined by immunohistochemistry. Western blotting was adopted to detect the effect of jatrorrhizine on the expression level of MABO protein in osteosarcoma cells. shRNA was used to interfere with the expression of MAOB, and its effect on the proliferation of osteosarcomacells was analyzed. Results Ten targets of jatrorrhizine on osteosarcoma, including MAOB, waspredicted by network pharmacology analysis. GSEA enrichment analysis showed that MAOB was related to the prognosis (P< 0. 05) and survival (log-rank P < 0. 05) of osteosarcoma. The viabilityof MG63 and U2OS cells decreased with the increase of the drug dose. The dose of 8 μmol / L was chosen for the follow-up functional test as the viability of osteosarcoma cells decreased by about50 % when the dose of jatrorrhizine reached 8 μmol / L. In vitro experiment showed that comparedwith those in the Control group, the cell proliferation rate of jatrorrhizine group was significantly reduced (P < 0. 05), and the number of invasion cells and migrating cells were significantly decreased (P< 0. 05), and the protein levels of Ki67, MMP2 and MMP9 were significantly downregulated (P< 0. 05). In vivo experiment showed that the growth rate of subcutaneous tumors in nudemice of jatrorrhizine group was significantly reduced ( P < 0. 05), and the weight and volume ofsubcutaneous tumors were lowered (P < 0. 05), and the expression level of Ki67 in tumor tissueswas significantly declined (P< 0. 05). Jatrorrhizine inhibited the expression of MAOB in osteosarcoma cells in a time and concentration-dependent manner in vitro (P < 0. 05). Knockdown of MAOBcould significantly inhibit the proliferation of osteosarcoma cells when compared with shNC group(P< 0. 05). Overexpression of MAOB could reverse the inhibitory effect of jatrorrhizine on the proliferation, invasion and migration of osteosarcoma cells (P< 0. 05). Conclusion The expression level of MAOB is related to the prognosis and survival of osteosarcoma. MAOB promotes cell proliferation, invasion and tumor metastasis. Jatrorrhizine inhibits the proliferation, invasion and migrationof osteosarcoma cells by inhibiting the expression of MAOB.

Anti-tumor Effect of Tetramethylpyrazine-containing Serum on Liver Cancer HepG2 Cells #br#
ZHANG Yifang, DAI Yi
2025, 22(1):  35-40.  doi:10.3870/j.issn.1672-8009.2025.01.006
Abstract ( 5 )   PDF (3433KB) ( 6 )  
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Objective To explore the effect and mechanism of tetramethylpyrazine ( TMP) -containing serum on proliferation, apoptosis and mitochondrial function of liver cancercells. Methods Serum from SD rats treated with 0, 30, 60, 120 mg / kg of TMP was collected andused to treat cells. Colony formation experiment and CCK-8 were employed to test the proliferation of HepG2 cells. Flow cytometry was performed to detect HepG2 cell cycle and apoptosis, mitochondrial membrane potential changes of HepG2 cells were measured by JC-1 through flow cytometry. Western blotting was used to detect the expression levels of PCNA, P27, cleaved caspase-3 (cas-3), Bax, Bcl-2 and Cyt C in HepG2 cells. SOD and MDA levels in HepG2 cells were detected by kits, and 2, 7-dichlorodiacetate (DCFH-DA) was used to determine the production of reactive oxygen species (ROS) in HepG2 cells. Results Compared with that of the control group, the TMP-containing serum of 60 and 120 mg / kg TMP groups significantly reduced the proliferation of HepG2 cells, and blocked cell cycle, moreover, HepG2 cell apoptosis rate was significantly increased and theantioxidant capacity was significantly reduced. Conclusion TMP-containing serum can inhibit theproliferation of liver cancer cells and induce apoptosis of liver cancer cells through a mitochondrialdependent pathway, and stimulate the generation of ROS to reduce the antioxidant capacity of cancer cells, thereby inhibiting the development of liver cancer.
Effect of Kaempferol on Inflammatory Response in Rats with Gestational Diabetes Mellitus via Regulation of IL-6 / STAT3 Signaling Pathway #br#
GUO Yanling, YANG Ying, JIANG Tiancong
2025, 22(1):  41-47.  doi:10.3870/j.issn.1672-8009.2025.01.007
Abstract ( 4 )   PDF (4916KB) ( 3 )  
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Objective To investigate the effect of kaempferol (Kpf) on inflammatory responsein rats with gestational diabetes mellitus (GDM) by regulation of the interleukin-6 (IL-6) / signaltransducer and activator of transcription 3 (STAT3) signaling pathway. Methods A rat model ofGDM was constructed by the combination of high fat and high sugar diets and intraperitoneal injection of streptozotocin ( STZ). GDM rats were then randomly divided into 5 groups: Model group, Kpf low-, medium-, and high-dose groups, and activator group ( IL-6 / STAT3 pathway activator rIL-6), with 12 rats in each group, another 12 rats without any special treatment as the control. Intraperitoneal injection of the corresponding drug was performed once a day until the 19th day of pregnancy. Roche blood glucose meter was applied to measure fasting blood glucose ( FBG) in rats. The pregnancy outcomes of rats in each group were analyzed. ELISA method was applied to determine the levels of fasting insulin (FINS) in rat serum and interleukin-6, interleukin-1β (IL-6, IL-1β), and tumor necrosis factor-α ( TNF-α) in placental tissues. Hematoxylin-eosin ( HE) staining was applied to observe pathological damage in rat placental tissues. TUNEL staining was applied to detect apoptosis in placental tissues. The expression levels of IL-6 / STAT3 pathway proteinsin placental tissues were detected by Western blotting. Results The values of FBG, FINS, HOMA-IR, fetal mouse weight, the levels of IL-6, IL-1β, TNF-α, the apoptosis rate of placental tissue cells, the expression levels of IL-6, p-STAT3 / STAT3 proteins in the Model group were increased when compared with those in the control group, while the live birth rate and the number ofoffspring were decreased when compared with those in the control group (P < 0. 05). The values ofFBG, FINS, HOMA-IR, fetal mouse mass, the levels of IL-6, IL-1β, TNF-α, the apoptosis rate of placental tissue cells, and the expression levels of IL-6, p-STAT3 / STAT3 proteins in the Kpf low-, medium-, and high-dose groups were decreased when compared with those in the Model group, while the live birth rate and the number of offspring were increased when compared withthose in the Model group (P < 0. 05). The changes of the above indicators in the activator group were reversed when compared to the Kpf high-dose group (P< 0. 05). Conclusion Kpf can alleviate placental inflammation and insulin resistance in GDM rats. Its mechanism may be related to the inhibition of IL-6 / STAT3 signaling pathway.

Effect of High Glucose-induced Oxidative Stress and Inflammatory Response on Apoptosis and Extracellular Matrix Metabolic Imbalance in Nucleus Pulposus Cells #br#
GUO Xiaoyan, CAO Sheng, WANG Lingling, XU Kun, YANG Jiaqi, YANG Xue, WANG Jing
2025, 22(1):  48-54.  doi:10.3870/j.issn.1672-8009.2025.01.008
Abstract ( 7 )   PDF (2204KB) ( 4 )  
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Objective To investigate the effect of high glucose treatment on apoptosis and extracellular matrix (ECM) metabolism in rat nucleus pulposus cells (NPC) and to preliminarily explorepossible underlying mechanisms. Methods NPC were isolated from lumbar spine tissues of maleWistar rats. NPC were divided into 6 groups: Control group, Glucose-treated groups (treated with 5mmol / L, 15 mmol / L, and 25 mmol / L glucose, respectively), high glucose + NAC group (treated with 25 mmol / L glucose and 3 mmol / L antioxidant NAC), high glucose + PDTC group (treated with 25 mmol / L glucose and 10 μmol / L NF-κB pathway inhibitor PDTC) . Cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Fluorescent probes were used to detect intracellular reactive oxygen species ( ROS) levels. Enzyme-linked immunosorbent assay was used to detect IL-1β, IL-6 and TNF-α levels. Western blotting was used to detect relevant protein expression levels. Results Compared to the cell viability and apoptosis in the control group, no significant change was observed in the 5 mmol / L and 15 mmol / L glucose groups, however, a significant decrease in cell viability and a significant increase in apoptosis were seen in the 25 mmol / L glucosegroup (P< 0. 05). The expression levels of Bcl-2-associated X protein (Bax), Caspase-3, MMP-3,MMP-9, MMP-13, A disintegrin and metalloproteinase with thrombospondin 4 (ADAMTS-4), and ADAMTS-5 were significantly decreased in the glucose + NAC and glucose + PDTC groups when compared with those in the 25 mmol / L glucose group, whereas the expression levels of Bcl-2, collagenⅡ (COLⅡ), and aggrecan were significantly increased (P< 0. 05). The intracellular ROS levelsand supernatant levels of the IL-1β, IL-6, and TNF-α in the glucose + NAC and glucose + PDTCgroups were significantly lower when compared with those in the 25 mmol / L glucose group (P< 0. 05). In addition, the cellular levels of p-P65 / P65 and p-IκBα / IκBα were significantly reduced in the glucose + NAC and glucose + PDTC groups when compared with those in the 25 mmol / L glucosegroup (P< 0. 05). Conclusion High glucose treatment promotes NPC apoptosis and ECM degradation by inducing oxidative stress and inflammatory responses, which involves the activation of ROS / NF-κB signaling pathway.

Effect of DJ-1 Protein Expression on Neurotransmitters Levels in Hippocampus of Depression Rats via PI3K / AKT Signaling Pathway #br#
LI Xiaoran, CAI Yunfeng, DING Zhaomeng, SUN Xiangsheng, LU Yuchen
2025, 22(1):  55-61.  doi:10.3870/j.issn.1672-8009.2025.01.009
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Objective To investigate the effect of DJ-1 protein expression on neurotransmitters levels in the hippocampus of depression rats. Methods Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) was used to detect the apoptosis in hippocampus. Enzyme linked immunosorbent assay was used to determine the levels of tumor necrosis factor-α ( TNF-α) and interleukin 6 (IL-6) in serum, and the levels of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and dopamine (DA) in hippocampus. Western blotting assay was used to detect the expression levels of DJ-1, PI3K, AKT, phosphorylated PI3K (p-PI3K), phosphorylated AKT ( p-AKT), Bcl-2 and Bcl-2 associated X protein ( Bax) in the hippocampus ofrats. Results Overexpression of DJ-1 significantly reduced the cell apoptosis rate in hippocampusand the levels of TNF-α and IL-6 in serum and the expression level of Bax in hippocampus, and upregulated the levels of 5-HT, 5-HIAA and DA in hippocampus and the expression levels of p-PI3K, p-AKT and Bcl-2 in hippocampus. However, the PI3K inhibitor LY294002 could partially reversethe protective effect of DJ-1 overexpression on neurons. Conclusion Overexpression of DJ-1 couldsignificantly inhibit inflammatory stress in the hippocampus of depression rats, reduce the apoptosis rate of neurons in the hippocampus, upregulate the levels of 5-HT, 5-HIAA and DA in the hippocampus, the mechanism may be related to the activation of PI3K / AKT signaling pathway.
MYH11 Activates the ERK / MAPK Signaling Pathway and Induces Growth and Metastasis of Laryngeal Squamous Cell Carcinoma Cells #br#
ZHONG Huacai, ZHENG Yuebin, YANG Yirong, YAN Bincheng, YI Wang, WANG Qian, WU Jun
2025, 22(1):  62-67.  doi:10.3870/j.issn.1672-8009.2025.01.010
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Objective To investigate the effect and mechanism of myosin heavy chain 11( MYH11 ) on the malignant biological behaviors of laryngeal squamous cell carcinomacells. Methods qRT-PCR was used to detect the expression level of MYH11 mRNA in laryngealsquamous cell carcinoma tissues and cells. Laryngeal squamous cell carcinoma cells TU686 were divided into 2 groups: si-MYH11 group and si-NC group. FD-LSC-1 cells were divided into 2 groups: MYH11 group and Vector group. CCK8, flow cytometry, wound-healing assay and Transwell assay were used to determine the cell proliferation, apoptosis, migration, and invasion abilities, respectively. Western blotting was used to detect the phosphorylation level of ERK1 / 2 and the expressionlevel of MAPK in each group of cells. Results MYH11 was highly expressed in laryngeal squamouscell carcinoma tissues and cells. The proliferation, migration, and invasion ability of TU686 cells inthe si-MYH11 group were significantly lower than those in the si-NC group ( P < 0. 05), and cell apoptosis was significantly higher than that in the si-NC group (P < 0. 01), the ERK1 / 2 phosphorylation level and MAPK expression level were significantly lower than those in the si-NC group (P< 0. 01). The proliferation, migration, and invasion ability of TU686 cells in the MYH11 groupwere significantly higher than those in the Vector group (P < 0. 05), and cell apoptosis was significantly lower than that in the Vector group ( P < 0. 01), the phosphorylation level of ERK1 / 2 and MAPK expression level were significantly higher than those in the Vector group (P < 0. 01). Conclusion MYH11 activates the ERK/ MAPK signaling pathway and promotes the proliferation, migration, and invasion of laryngeal squamous cell carcinoma cells.

Causal Relationship Between Gut Microbiota and Vitamin D Deficiency: A Two-sample Mendelian Randomization Study #br#
GUO Jing, LUO Jiamei , ZHU Junyong
2025, 22(1):  68-75.  doi:10.3870/j.issn.1672-8009.2025.01.011
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Objective To investigate the association between gut microbiota and vitamin D deficiency, and to identify specific gut microbial taxa related to the risk of vitamin D deficiency. Methods Data from genome-wide association studies (GWAS) on gut microbiota and vitaminD deficiency were summarized and analyzed. Inverse variance weighted (IVW) method was used for Mendelian randomization analysis to assess the causal relationship between gut microbiota taxa and vitamin D deficiency. Sensitivity analyses were conducted to evaluate heterogeneity, pleiotropy, androbustness of the results. Results In the absence of heterogeneity and horizontal pleiotropy, the IVW analysis method that showed Holdemania ( OR = 1. 524, 95 % CI = 1. 001-2. 231, P = 0. 049), Allisonella (OR = 1. 597, 95 % CI = 1. 095-2. 329, P = 0. 015), Escherichia-Shigella (OR = 2. 000, 95 % CI = 1. 156-3. 463, P = 0. 013), and Lachnospiraceae NC2004 group (OR = 2. 106, 95 % CI = 1. 178-3. 766, P = 0. 012) were positively associated with the risk of vitamin D deficiency. While the Lachnospira (OR = 0. 324, 95 % CI = 0. 124-0. 844, P = 0. 021) and Tyzzerella3 (OR = 0. 591, 95 % CI = 0. 406-0. 861, P = 0. 006) were negatively associated with the risk of vitamin D deficiency. Conclusion This study found significant correlations between the abundance of certain specific strains in the gut microbiota and the risk of vitamin D deficiency. This discovery may provide new potential targets for the prevention and treatment of vitamin D deficiency.

Identification of Differentially Expressed Glycolysis-related Genes and Establishment of Prognostic Model for Gastric Cancer by Bioinformatics #br#
XU Juan, HU Wanqi
2025, 22(1):  76-83.  doi:10.3870/j.issn.1672-8009.2025.01.012
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Objective To explore the expression of glycolysis-related genes ( GRGs) in gastric cancer by bioinformatics, and the relationship between the established risk scoring model andprognosis of gastric cancer. Methods The genes expression profiles and clinical feature data of gastric cancer samples were downloaded from the Cancer Genome Atlas (TCGA) database. The GRGs set was obtained from the GSEA database. We used “ limma” packets to identify differentially expressed GRGs in gastric cancer tissues, and used univariate Cox regression analysis to screen for prognosis related GRGs. Then, LASSO regression analysis was used to construct a prognosis prediction model based on the GRGs. A nomogram was developed based on the independent prognostic risk factors determined by Cox regression analysis. Finally, the correlations between 22 types of infiltrating immune cells and the GRGs or risk scoring models were analyzed. Results Twenty-one differentially expressed GRGs were identified, which were mainly enriched in the alcohol metabolism andtyrosine metabolism pathways. Finally, 5 prognostic related glycolytic genes ( ADH1B, ADH4, CLDN9, VCAN, and LHX90) were selected by LASSO and Cox models and were used to constructa gene signature for gastric cancer prognosis prediction. The overall survival of gastric cancer patients with low-risk scores is significantly better than that of gastric cancer patients with high-risk scores. The ROC curve analysis showed that the values of area under the curve (AUC) of the abovemodel to predict the 1-year, 3-year, and 5-year survival for the gastric cancer patients were 0. 602,0. 680, and 0. 802, respectively. The effectiveness of this model to predict the survival of gastriccancer patients was better than that of using tumor staging and grading. Univariate and multivariate Coxanalysis showed that the prognostic model, age, gender, tumor stage and tumor grade were independent prognostic factors for gastric cancer. Based on these prognostic factors, a Nomogram was constructed to predict the survival of gastric cancer patients. Finally, we found that the proportion of CD8T cells and helper follicular T cells was significantly reduced in the high-risk group, while the proportion of M0 macrophages and M2 macrophages was significantly higher in the high-risk group than inthe low-risk group. The proportion of helper follicular T cells was negatively correlated with the expression levels of ADH1B and VCAN and the risk scores. The proportion of M2 macrophages was positivelycorrelated with the expression level of VCAN and the risk scores. Conclusion The 5 GRGs screenedout in this study are related to the prognosis of gastric cancer, which can be used for the prognosis ofgastric cancer patients and may be used as potential therapeutic targets for gastric cancer.

Research Progress on Application of Helminth Proteomics #br#
YI Ling, PENG Peiying, HE Ping,
2025, 22(1):  84-90.  doi:10.3870/j.issn.1672-8009.2025.01.013
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Proteomics studies the composition, structure, function, and interactions of allproteins in living organisms. Helminth infections have a serious impact on the health of hundreds of millions of people worldwide and result in significant economic losses for the livestock industry. With the continuous development and in-depth study of proteomics technologies, remarkable progress has been made in the application researches of helminth proteomics. This review summarizes the representative researches on helminth proteomics, the progress of proteomics technology studies, and the application on diagnosis, prevention, and control of helminthiasis, to provide new ideas and methods for screening diagnostic markers and drug targets for helminthiasis.
The Role of Astrocytes in Subarachnoid Hemorrhage #br#
SUI Chen, SUN Xingang
2025, 22(1):  91-96.  doi:10.3870/j.issn.1672-8009.2025.01.014
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Subarachnoid hemorrhage (SAH) is a cerebrovascular disease that is characterizedby a high rate of disability and mortality. Astrocytes play a crucial role in brain injury and recovery following SAH. This paper summarizes the activation and polarization of astrocytes after SAH, their participation and mediation in early brain injury and delayed cerebral ischemia after SAH, and the extensive crosstalk between astrocytes and other brain cells, such as neurons, microglia, and vascular endothelial cells after SAH. In addition, the relevant targets and therapeutic methods for regulating astrocyte function after SAH are also listed here, offering some novel strategies for future translational therapies to alleviate the severe consequences of SAH.
Research Progress on Azole Resistance in Aspergillus fumigatus Efflux Pumps #br#
WANG Juan, MA Yan
2025, 22(1):  97-100.  doi:10.3870/j.issn.1672-8009.2025.01.015
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Aspergillus fumigatus ( A. fumigatus) is an opportunistic pathogen widely found innature and can cause invasive aspergillosis (IA), with a high mortality rate in immunocompromisedpatients. Triazoles are the first-line therapy for IA, but in recent years, the number of azole-resistant Aspergillus fumigatus isolates is increasing worldwide, which greatly threatens the life and healthof patients. Efflux pumps are composed of transmembrane proteins that can expel unwanted substances out of cells, which is an important mechanism in protecting microorganisms. In addition, many studies suggest that efflux pumps can also mediate microbial drug resistance. This paper summarizes the recent progress on the function and regulation mechanism of the drug efflux pump ofA. fumigatus, which provides a theoretical basis for the deep understanding of the resistance mechanism in A. fumigatus and the screening of new targets of anti-infective drugs.
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