Acta Universitatis Medicinalis Anhui

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Anhui Provincial Education Department

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Anhui Medical University

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Weng Jianping

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Editorial Board of Acta Universitatis Medi-cinalis Anhui Meishan Road , Hefei 230032

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China Code No . MO5933

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ISSN 1000 - 1492

CN 34 - 1065/R

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Study on the role and mechanism of SDC2 expression in regulating ferroptosis and cervical cancer

Yao Xueqin , Xiao Xuelian , Luo Qiying , Chang Deping , Gao Yan

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.007

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abstract:
Abstract Objective To investigate whether syndecan-2 (SDC2) can affect the proliferation , invasion and migra- tion of cervical cancer cells by regulating ferroptosis and its possible mechanism . Methods Normal cervical epithe- lial cells H8 and cervical squamous carcinoma cells C33A were cultured and divided into H8 group and C33A group . C33A cells were cultured and divided into control group , low SDC2 expression group , SDC2 + ferroptosis inhibitor(ferrostation-1) group and SDC2 + ferroptosis inducer (erastin) group . Western blot was used to detect the protein levels of SDC2 , solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) . RT-qPCR was used to detect the SDC2 mRNA level in C33A cells . ELISA kits were used to detect the levels of re- active oxygen species (ROS) , glutathione (GSH) and ferrous ion ( Fe2 + ) in C33A cells . The cloning ability of C33A cells was detected by plate cloning. The migration ability of C33A cells was detected by scratch test. Tran- swell assay was used to detect the invasion ability of C33A cells . Results Compared with H8 group , the protein and mRNA expressions of SDC2 , SLC7A11 and GPX4 in C33A group increased (P < 0. 05) . Compared with the control group , the proliferation ability , migration ability and invasion ability of C33A cells in the low SDC2 group decreased(P < 0. 05) , the protein and mRNA expressions of SLC7A11 and GPX4 in C33A cells decreased (P < 0. 05) , and the GSH level decreased . ROS and Fe2 + levels increased (P < 0. 05) . Compared with the low SDC2 group , the protein and mRNA expressions of SLC7A11 and GPX4 increased (P < 0. 05) , the GSH level increased , and the ROS and Fe2 + levels decreased ( P < 0. 05) in the low SDC2 + ferrostation-1 group . Compared with the control group , the proliferation ability , migration ability and invasion ability of C33A cells with low SDC2 + erastin expression decreased (P < 0. 05) . Conclusion The expression of SDC2 increases in C33A cervical cancer cells . Low expression of SDC2 can activate SLC7A11 /GPX4 pathway mediated ferroptosis , thereby reducing the prolifera- tion , invasion and migration of C33A cells .

Study on the antagonistic activity of Lactococcus garvieae SHAMU-LG6 against Staphylococcus

Weng Shengnan1 , Leng Guiyun1 , Liu Ying2 , Wang Yawu1 , Li Xin1 , Yao Jie1 , Zhou Qiang1 , Tang Wei 1

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.002

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Role of the iNOS/IRS1/AKT/GSK-3 βsignaling pathway in chronic intermittent hypoxia-induced insulin resistance

Jin Meina1 , Zhou Xueli 1 , Li Haibo 1 , Bai Wei 1 , Jia Chuxuan1，Gao Li 1 , Ren Lijue2 , Chen Qingyu3 , Wang Rui4 , Li Hua5 , Wei Cuiying1

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.004

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abstract:
Abstract Objective Pathological changes and inducible nitric oxide synthase ( iNOS), phosphorylated insulin receptor substrate 1 serine 307 (p-IRS1ser 307), phosphorylated protein kinase B serine 473 ( p-AKTser 473), glycogen synthase kinase-3 β(GSK-3 β), and gluconeogenic synthase (GS) proteins were observed in the liver of rats under the condition of chronic intermittent hypoxia-replicated oxygen in control . And to explore the role of iN- OS/IRS1 /AKT/GSK-3 βsignaling pathway in chronic intermittent hypoxia-induced insulin resistance . Methods Forty SD rats were randomly divided into a control group ( NC group) and an experimental group ( CIH group), with 20 rats in each group . The NC group was placed in a normoxic environment for 12 weeks , while the CIH group was first subjected to intermittent hypoxia for 8 weeks , and then resumed normoxic rearing until the 12th week . Fasting blood glucose (FBG) and fasting insulin (FINS) were measured at baseline , week 8 and week 12 , and liv- er tissues were taken for pathology and measurement of iNOS , p-IRS1ser 307 , p-AKTser 473 , GSK3 βand GS lev- els , to compare the differences between groups . Results At baseline , there was no significant difference in liver pathology between the two groups , and the observed indexes were not statistically significant ( P > 0. 05 ); at 8 weeks , compared with the NC group , liver pathology in the CIH group showed significant disorganization of hepatic blood sinusoids and hepatocyte cords , obvious hepatocyte edema , smaller nuclei , increased lymphocyte infiltration , and a small number of fat vacuoles , significantly higher levels of FBG , FINS , insulin resistance index ( HOMA- IR), iNOS mRNA , p-IRS1ser 307 protein , GSK-3 βprotein levels , and decreased p-AKTser 473 protein and GS protein levels , all of which were statistically significant (all P < 0. 05) . IRS1ser 307 protein , GSK-3 βprotein lev- els were increased , p-AKTser 473 protein and GS protein levels were decreased , and the differences were statisti- cally significant (all P < 0. 05); at 12 weeks , no lymphocyte infiltration was seen in the CIH group compared with that of the NC group and fat vacuoles significantly increased , and there was no improvement in the other pathological damage that had already occurred , and the levels of p-AKTser 473 protein significantly increased . AKTser 473 protein level significantly increased , p-IRS1ser 307 protein and GS protein levels were significantly reduced , all of which were statistically significant (all P < 0. 05), and the rest of the observational indexes were not statistically significant. Pearson′s correlation analysis showed that HOMA-IR of CIH group was significantly positively correlated with the lev- els of iNOS mRNA , p-IRS1ser 307 protein , and GSK-3βprotein at 8 weeks ( r = 0. 874 , 0. 817 , 0. 872;all P < 0. 05), and significantly negatively correlated with the levels of p-AKTser 473 protein and GS protein ( r = - 0. 886 , - 0. 879;all P < 0. 05) . Conclusion Chronic intermittent hypoxia can lead to hepatic pathological damage that can- not be reversed even by reoxygenation interventions and may mediate the development of insulin resistance by upregu- lating the IRS1/AKT/GSK-3βsignaling pathway through the upregulation of iNOS mRNA expression.

Whole genome sequencing of Bifidobacterium animalis subsp. lactic B4 and analysis of its probiotic properties

Ding Ruipei 1 , Liu Chengzhong2 , Shi Cancan2 , Zhang Huiyu1 , Dai Yiping2 , Mu Ruxue2 , Li Zilong2 , He Maozhang2 , Li Zhuojun3

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.010

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Effect of WTAP on collagen deposition in bleomycin-induced pulmonary fibrosis

Zhang Yunsen1 , 2 , Liu Zhenyu1 , 2 , Liu Zhiyan1 , 2 , Lin Lichan1 , 2 , Sha Jiming3 , Tao Hui 1 , 2 , Chen Qi 1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.011

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abstract:
Abstract Objective To explore the effect of Wilms ′tumor 1-associated protein (WTAP) on tissue collagen dep- osition in pulmonary fibrosis caused by bleomycin . Methods 60 mice were randomly divided into four groups : control group ( Control group) , Bleomycin-induced pulmonary fibrosis group ( BLM group) , pulmonary fibrosis lentivirus empty vector control group ( BLM + LV-NC group) , pulmonary fibrosis WTAP lentivirus group virus group (BLM + LV-WTAP group) . Experimental pulmonary fibrosis mouse model was established by subcutaneous injection of bleomycin (35 mg/kg) into the abdomen , twice a week for a total of 8 times . After modeling , Western Blot was used to detect the protein expression of fibrosis-related markers α-smooth muscle actin ( α-SMA) , type I collagen (Collagen Ⅰ ) , fibronectin (Fibronectin) , and WTAP protein . Masson staining and Sirius Red staining were used to detect collagen deposition . RT-qPCR was used to detect WTAP mRNA expression , WTAP lentivirus infection effect , and Collagen Ⅰ mRNA expression . Results Compared with the Control group , the expression of pulmonary fibrosis markers α-SMA (P < 0. 001) , Collagen Ⅰ (P < 0. 001) , and Fibronectin (P < 0. 01) protein in the BLM group all increased . Masson staining (P < 0. 001) and Sirius Red staining (P < 0. 001) confirmed that significant collagen deposition occurred in the lung tissue of the BLM group . In addition , the expression of WTAP protein in the lung tissue of the BLM group increased (P < 0. 01) . Compared with the Control group , the expres- sion of WTAP mRNA in the BLM group increased (P < 0. 001) . Compared with the BLM + LV-NC group , the ex- pression of WTAP mRNA in the tissues of the BLM + LV-WTAP group decreased (P < 0. 001) , proving that virus infection is effective . After infection with WTAP lentivirus , collagen fiber deposition decreased (P < 0. 001) , Col- lagen Ⅰ mRNA (P < 0. 001) level decreased , and protein (P < 0. 001) expression decreased in the BLM + LV- WTAP group . Conclusion Knocking down of WTAP can reduce collagen deposition in bleomycin-induced pulmo- nary fibrosis tissue in mice and improve experimental pulmonary fibrosis .

BRD4 regulates alveolar epithelial-mesenchymal transition through HMGB1/TGF-β1/Smad pathway

Chen Ruru1 , Han Lu1 , He Hailan1 , 2 , Hao Xiaohui 1 , 2 , Liu Heliang1 , 2 , Guo Lingli 1 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.009

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abstract:
Abstract Objective To investigate the mechanisms of bromodomain-containing protein 4 (BRD4) in TGF-β1-in- duced epithelial-mesenchymal transition in alveolar type II epithelial cells . Methods MLE-12 cells were stimula- ted with different concentrations (5 ng/ml , 10 ng/ml) of TGF-β1 for 48 h to establish an EMT cell model . The cells were pretreated with 50 nmol/L BRD4 inhibitor JQ-1 , 100 μmol/L high mobility group box 1 protein (HMGB1)inhibitor glycyrrhizin acid (GA) , and 3 μg/ml rHMGB1 . The experimental groups were divided as fol- lows : control group , TGF-β1 group , JQ-1 group , JQ-1 + TGF-β1 group , GA group , GA + TGF-β1 group , and JQ - 1 + TGF-β1 + rHMGB1 group . The effect of JQ-1 on cell viability was examined using cell counting kit-8 ( CCK- 8) . The protein expression levels of CDH1 , ZO-1 , Vimentin , α-SMA , BRD4 , HMGB1 , TGF-β1 , Smad2/3 and p-Smad2/3 were detected by Western blot. The cell migration ability was detected by a scratch test. Results Compared with the control group , the levels of Vimentin and α-SMA in the TGF-β1 group increased , and the levels of CDH1 and ZO-1 protein decreased , suggesting that the EMT model was successfully established . In this model , the expression of BRD4 and HMGB1 significantly increased . Different concentrations of JQ-1 could inhibit the cell viability of MLE-12 in a concentration-dependent manner. Both JQ-1 and GA could effectively alleviate TGF-β1-in- duced EMT , and reduce the increase in HMGB1 expression and the activation of TGF-β1/Smad2/3 pathway caused by TGF-β1 . Moreover , rHMGB1 treatment could reduce the effects of JQ-1 on EMT and the TGF-β1/Smad2/3 pathway . Additionally , both JQ-1 and glycyrrhizin could effectively decrease TGF-β1-induced cell migration , whereas rHMGB1 could alleviate the inhibitory effect of JQ-1 on the rate of cell migration . Conclusion BRD4 can regulate epithelial-mesenchymal transition in alveolar type II epithelial cells via HMGB1 /TGF-β1/Smad2/3 signa- ling cascade , and BRD4 may be a potential target for inhibition of pulmonary fibrosis .

Association between PROS1 gene polymorphism and recurrent spontaneous abortion in Baotou Han population

Zhao Pingping1 , 2 , Wu Di3 , Li Dechun2 , Wang Yanguo4

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.008

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Study on the mechanism of long non-coding RNA LUCAT1 regulating the malignancy of pancreatic cancer MIA PaCa-2 cells

Ye Mengjie , Qu Weiwei , Luo Guangtao

DOI: 10.19405/j.cnki.issn1000-1492.2025.02.001

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