Acta Universitatis Medicinalis Anhui

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Anhui Medical University

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Weng Jianping

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Paeoniflorin alleviates cisplatin and lansoprazole-induced acute kidney inj ury by inhibiting necroptosis

Xu Qi , Luo Xiaomei , Zhu Wei , Li Yuanyuan , Wu Yonggui

DOI: 专辑：医药卫生科技

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abstract:
Abstract Objective To investigate the effects of paeoniflorin (Pae) on acute kidney injury ( AKI) and mouse renal tubular epithelial cell ( mRTEC) damage induced by lansoprazole (LPZ) and cisplatin (CIS) through in vivo and in vitro experiments . Methods The C57BL/6J mice or mRTECs were divided into four groups : normal control (NC) group , NC + LPZ group , CIS group , and CIS + LPZ group . Serum creatinine (CRE) and blood urea nitro- gen (BUN) levels in mice were measured , and kidney pathology was observed with HE staining. Western blot , im- munohistochemistry , and immunofluorescence were used to detect the expression levels of kidney injury molecule-1 (KIM-1) and receptor-interacting protein kinase (RIPK) 1 , RIPK3 , and mixed lineage kinase domain-like protein (MLKL) . Subsequently , C57BL/6J mice or mRTECs were divided into six groups : NC group , NC + Pae group , CIS + LPZ (M) group , and CIS + LPZ + Pae ( M + Pae) group . Serum CRE and BUN levels in each group were measured , kidney pathology was observed with HE staining , and ultrastructural changes in the kidney were ob-served with transmission electron microscopy. The KIM-1 and necroptosis-related protein expression levels were de- tected by Western blot , immunohistochemistry , and immunofluorescence . Results Compared with the NC group , CRE and BUN levels were elevated in the CIS group , and these levels were further increased after LPZ intervention (all P < 0. 001) . Compared with the CIS group , renal tubular dilation and brush border loss were evident in the CIS + LPZ group based on HE staining of kidney tissue (P < 0. 001) . Compared with the NC group , the expres- sion levels of KIM-1 , RIPK1 , RIPK3 , and MLKL in the renal tissues of mice in the CIS group increased (all P < 0. 001) , and compared with the CIS group , The expression levels of KIM-1 , RIPK1 , RIPK3 and MLKL in the re- nal tissues of mice in the CIS + LPZ group increased (all P < 0. 001) . After Pae treatment , compared with group M , the expression levels of CRE , BUN , KIM-1 , RIPK1 , RIPK3 and MLKL in each group of mice decreased sig- nificantly and in a dose-dependent manner (all P < 0. 001) . Conclusion LPZ promotes CIS-induced AKI by en- hancing necroptosis in renal tubular epithelial cells , and Pae can improve CIS and LPZ-induced AKI by inhibiting necroptosis .

Effects of LSS function deficiency on intestinal function in NAFLD model mice

Bai Hongmei1, Yang Zhen1, Hu Weikang1 , Wang Zihan1, Zhou Wenjing1, He Qingya1, Zhong Jian1, Li Mingcong2, Liu Li3, Zhang Chaoyang3, Zhang Sumei1, Zhang Shengquan1

DOI: 专辑：医药卫生科技

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abstract:
Abstract Objective To investigate the effect of loss of function of lanosterol synthase(LSS) on intestinal function in a mouse model of non-alcoholic fatty liver disease(NAFLD) induced by a high-fat diet. Methods LSS heterozygous knockout C57 mice (LSS+/-) were established using the CRISPR/CAS9 system. After being fed a high-fat diet with 60% fat content for 6 months, the fat deposition in liver tissues was detected by HE and Oil red O staining, the morphological changes of small intestine tissue were detected by HE staining. The changes in total cholesterol content in intestinal tissue were detected by kits. The gastrointestinal motility function of mice was detected by phenol red paste. The intestinal permeability was detected by Evans blue staining, and the expression of lanosterol synthase (LSS), tight junction protein (Claudin)-1, Claudin-5, platelet glycoprotein IV (CD36), and Niemann-Pick C1-like 1 (NPC1L1) proteins in small intestinal tissues were detected by Western blot. Results The results of HE and Oil red O staining of liver tissues showed that liver fat deposition in LSS knockdown mice was lower than that in wild-type mice in the high-fat diet group. The total cholesterol content in intestinal tissue of LSS gene knockout mice decreased (P<0.01), but no morphological differences were observed between the two groups of mice by HE staining of intestinal tissues. The gastrointestinal motility function of LSS gene knockout mice did not show significant changes. The intestinal permeability of LSS gene knockout mice in the high-fat diet group decreased as detected by Evans blue (P < 0.05). The expression levels of Claudin-5 protein in the intestinal tissue of LSS gene knockout mice in the high-fat diet group increased (P<0.05), while the expression of LSS in the intestinal tissues of LSS knockout mice decreased (P<0.05). Conclusion In the NAFLD model induced by a high-fat diet,LSS gene knockout reduces liver fat deposition induced by a high-fat diet and improves intestinal barrier function by regulating cholesterol metabolism in intestinal tissues and up-regulating the expression of tight junction protein-5.

RNA-seq-based screening of autophagy-related genes during lung infection by highly antibiotic-resistant and highly virulent Staphylococcus aureus

Zha Jinhong1,2, Kuang Qi1,2, Wu Chengxi2, Zhu Xiaoyu2, Su Duo2, Zhang Lili2, Lü Meng2, Hu Lingfei2, Zhou Dongsheng2, Yang Wenhui1,2

DOI: 专辑：医药卫生科技

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abstract:
Abstract Objective To identify autophagy-related genes involved in pulmonary infection caused by the highly drug-resistant and virulent methicillin-resistant Staphylococcus aureus strain USA300 (USA300), and to explore the underlying molecular mechanisms, thereby providing potential targets for immunotherapy. Methods The GSE220943 dataset of a USA300-induced pulmonary infection mouse model was obtained from the GEO database. Differentially expressed genes (DEGs) were identified using the DESeq2 package. Autophagy-related genes (ARGs) were retrieved from the MSigDB and Autophagy databases. Weighted gene co-expression network analysis (WGCNA) was performed to construct gene co-expression modules. Genes overlapping among DEGs, ARGs, and WGCNA modules were identified as autophagy-related DEGs. Gene Ontology (GO) enrichment analysis was conducted using the clusterProfiler R package, while Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was performed via the Metascape platform. Immune cell infiltration was analyzed using the ImmuCellAI-mouse website. A protein–protein interaction (PPI) network was constructed using the STRING database, and hub genes were identified through topological analysis in Cytoscape. ROC curves were plotted via the website https://www.bioinformatics.com.cn. Finally, key gene expression was validated in mouse lung tissues by real-time quantitative reverse transcription PCR (RT-qPCR).Results A total of 6 135, 4 075, 3 680, and 2 342 differentially expressed genes (DEGs) were identified at 12, 24, 48, and 96 hours post-infection, respectively. By integrating DEGs,autophagy-related genes (ARGs), and WGCNA modules, 19 autophagy-related DEGs were identified. GO and KEGG enrichment analyses indicated that these genes were mainly involved in CD4⁺ T cell activation and regulation, innate immune responses, and autophagosome membrane formation. Immune infiltration analysis revealed that innate immune cells such as neutrophils and dendritic cells predominated during the early phase of infection, while γδ T cells and M2 macrophages became more prominent in the later stages. PPI network analysis identified 12 hub autophagy-related genes, among which three upregulated key genes (Eif2ak2, Ikbke, and Nfkbiz) were further confirmed. The area under the ROC curve (AUC) for all three genes was 1.0.RT-qPCR validation demonstrated significantly elevated expression of these three genes in lung tissues at 24 hours post-infection (all P<0.05). Conclusion Eif2ak2, Ikbke, and Nfkbiz may be involved in the pulmonary infection caused by USA300 by promoting autophagy and hold promise as potential targets for immunotherapy.

Research progress on ferroptosis in the intervertebral disc degeneration

Liu Jianjun1,2, Yu Shuisheng1,2, Jing Juehua1,2, Tian Dasheng1,2

DOI: 专辑：医药卫生科技

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Therapeutic evaluation of extracellular vesicles produced by Aspergillus flavus in Aspergillus flavus infections

Zhou Jianhong1,2, Wang Li1,2, Yao Langxuan1,2, Zhang Chunlin1,2 , Jiang Yinhui1,2

DOI: 专辑：医药卫生科技

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The role of corticosterone pretreatment on LPS-activated microglia and the inhibitory effect of Biochanin A

Niu Gengchen1,2, Wang Jun1, Zhang Yue1, Yin Yanyan1

DOI: 专辑：医药卫生科技

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abstract:
Abstract Objective To investigate the regulatory effect of corticosterone (CORT) pretreatment on the activation of microglia by lipopolysaccharide (LPS) and the inhibitory effect of Biochanin A (Bio A) on microglia activation. Methods The MTT method was used to select the optimal concentrations for LPS, CORT and Bio A on BV2 cells; BV2 cells were divided into 5 groups: Control group, CORT (50 nmol/L) group, LPS (1 μg/mL) group, LPS (1 μg/mL) + CORT (50nmol/L) group, and LPS (1 μg/mL) + CORT (50 nmol/L) + Bio A (5 μmol/L) group; Except for the control group, each group was first incubated with CORT (50 nmol/L) for 2 h, and then each group was co-incubated with the corresponding concentrations of LPS (1 μg/mL) and BioA (5μmol/L) for 36 h; DCFH-DA probe method was used to detect reactive oxygen species (ROS) content; Western blot was used to detect the protein expression levels of inflammatory cytokines,5-hydroxytryptamine(5-HTT), glucocorticoid receptor (GR), mineralocorticoid receptor (MR), NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and cysteine-aspartic protease 1 (Caspase-1) Results Compared with the CORT (50 nmol/L) and LPS (1 μg/mL) groups, cells in the CORT (50 nmol/L)+ LPS (1 μg/mL) group showed increased cell viability, higher levels of ROS, and increased levels of inflammatory cytokines, NLRP3, ASC, and Caspase-1 protein expression (P<0.05);Compared with the CORT (50 nmol/L) + LPS (1 μg/mL) group, the CORT (50 nmol/L) + LPS (1 μg/mL) + Bio A (5 μmol/L) group showed decreased cell viability, decreased levels of ROS, and decreased protein expression of inflammatory cytokines, NLRP3, ASC and Caspase-1 proteins (P<0.05 ).Conclusion A low dose of CORT pretreatment reinforces LPS-induced BV2 cell activation; Bio A inhibits CORT-pretreated LPS-induced BV2 cell activation. The mechanism of which may be related to the inhibition of NLRP3 inflammasome activation.

KobophenolA inhibits LPS-induced macrophage M1 polarization via Prdx6

Chen Tianyu1,2, Wang Hao1,2 ,Wang Jinhong1,2 , Zhao Yingjie1,2, Zhou Renpeng1,2, Hu Wei1,2, Lu Chao1,3

DOI: 专辑：医药卫生科技

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abstract:
Abstract Objective To explore the effects and mechanisms of Kobophenol A (KPA) on lipopolysaccharide (LPS)-induced M1 macrophage polarization, and to provide a theoretical basis for the treatment of inflammatory immune diseases and the development of new drugs. Methods The M1 macrophage polarization model of RAW264.7 was established by LPS induction, and the Prdx6 knockdown model was constructed using the Prdx6 inhibitor MJ33 and Prdx6-siRNA. RAW264.7 cells, a mouse macrophage cell line, were treated with various concentrations of KPA. Cell viability was assessed using the CCK-8 assay. The expression levels of peroxiredoxin 6 (Prdx6) and M1 macrophage polarization-related proteins, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), were detected by Western blot and immunofluorescence staining. The expression levels of Prdx6 and M1 macrophage polarization-related genes iNOS, interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α), were measured by RT-qPCR. Flow cytometry was employed to detect the expression of CD86, a marker of M1 macrophages. Results Compared with the LPS-induced M1 macrophage polarization model, KPA significantly reversed the morphological changes of M1 macrophage polarization in RAW264.7 macrophages and decreased the expression of M1 macrophage polarization-related proteins iNOS, COX-2, CD86 and related genes iNOS, IL-6, TNF-α (all P<0.05). In addition, LPS significantly downregulated the expression of Prdx6 in RAW264.7 macrophages, while KPA upregulated the expression of Prdx6. Moreover, treatment with the Prdx6 inhibitor MJ33 significantly upregulated the expression of iNOS, a marker of M1 macrophage polarization, in RAW264.7 macrophages, whereas treatment with KPA significantly downregulated the expression of iNOS (all P<0.05). Conclusion KPA inhibits LPS-induced M1 polarization of RAW264.7 macrophages by upregulating the expression of Prdx6.

Csf1r-Cre-mediated yellow fluorescent protein can effectively label tissue-resident macrophages in various tissues

Li Xiaoyu1, Zhao Dianyuan2,3, Zhang Shengquan1, Yang Jing1,2,3, Tang Li1,2,3

DOI: 专辑：医药卫生科技

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