Acta Universitatis Medicinalis Anhui

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Anhui Provincial Education Department

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Anhui Medical University

Editor-in-chief

Weng Jianping

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

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Hefei Post Office of Anhui Province, China

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26 - 36

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China Code No . MO5933

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￥:10.00/Issue, 120.00/Year

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ISSN 1000 - 1492

CN 34 - 1065/R

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(0551)65161103, 65161192

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Cloning , expression , and functional analysis of capsule-specific depolymerase targeting carbapenem-resistant Klebsiella pneumoniae

Yan Tao1 , 2 , Wang Na3 , Wang Qiuyan1 , Ma Chengcheng1 , Teng Xuan1 , Yu Kexue 1 , Ge Honghua3 , Liu Zhou1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.013

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Construction and phenotypic study of heterozygous knockout mice of tumor necrosis factor receptor associated factor 2

Wang Weikang , Zuo Shujun , Gu Jintao , Guo Fuyuan , Guo Haozhou , Han Chenchen , Wei Wei

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.018

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abstract:
To generate heterozygous TRAF2 knockout mice , the CRISPR/Cas9 technology was suc- cessfully employed . These mice were served as a valuable model to explore the pathological mechanisms underlying inflammatory and immune disorders mediated by abnormal TNF-α-TRAF2 signaling and to develop new therapeutic targets . Methods A vector targeting the knockout of the TRAF2 gene was constructed . Lead RNA and Cas9 Mrna were introduced into the fertilized eggs of C57BL/6JGpt mice through microinjection to mediate the TRAF2 gene mutation in mice . The mouse tail protein was extracted and the genotype of the F0 generation was determined by PCR and Western blot. TRAF2 + / - mice were successfully obtained . F0 generation mice were backcrossed with C57BL/6JGpt wild-type mice to obtain stable TRAF2 + / - mice for propagation and subsequent experiments . The body weight of TRAF2 + / - mice was detected; Western blot was used to detect the expression of TRAF2 in the spleen , liver and kidney tissues of TRAF2 + / - mice . The development of spleen , liver and kidney tissues in TRAF2 + / - mice was detected by HE staining. Results PCR identification using specific primers demonstrated that TRAF2 + / - mice exhibited a target band at 679 bp . Western blot analysis results indicated that , compared with the WT group , the expression of TRAF2 in the tail protein of TRAF2 + / - mice was significantly reduced( P < 0. 01) . TRAF2 + / - mice had a lower body weight compared to their littermate WT mice(P < 0. 05) . Western blot analysis showed that , relative to the WT group , the expression of TRAF2 protein in the spleen , liver , and kidney tissues of TRAF2 + / - mice was decreased(P < 0. 01) . HE staining results indicated that there were no significant differences in cellular morphology in the spleen , liver , and kidney tissues between TRAF2 + / - mice and WT mice . Conclusion The successful construction of TRAF2 + / - mice has provided an important animal model for exploring the role of TRAF2 in developmental regulation , revealing the mechanism of inflammatory immune diseases mediated by abnor- mal TNF-α-TRAF2 signaling , and screening related drug targets .

Expression and significance of kynurenine-3-monooxygenase in peripheral blood mononuclear cells and synovial tissue of patients with rheumatoid arthritis

Zong Xuemei 1 , Lin Qianqian1 , Chen Yuelan1 , Wang Xinming2 , Wei Wei 1 , Yan Shangxue1 , 3 , Chang Yan1 , 3

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.008

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abstract:
To investigate the expression and clinical significance of kynurenine-3-monooxygenase (KMO) in peripheral blood mononuclear cells ( PBMC ) , synovial tissue , and fibroblastic-like synovial cells (FLS) of rheumatoid arthritis (RA) patients . Methods Peripheral blood samples from 25 healthy control (HC) individuals and 25 patients diagnosed with RA were collected , and real-time fluorescence quantitative PCR and Western blot were used to detect KMO gene and protein expression in PBMC of RA and HC groups , and to analyze the correlation between the expression level of the KMO gene in the PBMC of the RA patients and the indexes of the laboratory tests . Meanwhile , immunohistochemistry and immunofluorescence were used to detect KMO expression in synovial tissue and FLS in RA and HC groups . Results ① KMO gene and protein expression in PBMC of RA group were higher than that of HC group , and the difference was statistically significant (P < 0. 001) . ② The level of KMO gene expression in PBMC of RA group was positively correlated with disease activity index 28 score , blood sedimentation , and rheumatoid factor ( rs = 0. 417 , P = 0. 038 ; r = 0. 545 , P = 0. 005 ; rs = 0. 433 , P = 0. 031) , and had no correlation with C-reactive protein and anti-cyclic citrullinated polypeptide antibody . ③ KMO expres- sion in synovial tissue of RA group was higher than that of HC group , and the difference was statistically significant (P < 0. 01) ; KMO expression in FLS of synovial tissue of RA group was higher than that of HC group , and the difference was statistically significant ( P < 0. 001) . Conclusion KMO expression increases in PBMC , synovial tissue and FLS of RA patients , and the level of KMO gene expression is correlated with the disease activity of RA patients , suggesting that KMO may promote the course of RA .

Effects and mechanism of astragalus mongholicus extract on lung inj ury in rats with rheumatoid arthritis induced interstitial lung disease

Zhao Yue , Yang Jinliang , Luo Huan , Xi Wenxiu , Wang Junlu , Zheng Xuejun

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.002

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abstract:
To investigate the effects of astragalus mongholicus extract ( AME) on lung injury and the myeloid differentiation factor 88 ( MyD88) /Toll-like receptor 4 ( TLR4 ) /nuclear factor kappa B ( NF-κB) p65 pathway in rheumatoid arthritis induced interstitial lung disease (RA-ILD) rats . Methods SD rats were randomly divided into a control group , RA-ILD group , low-dose AME group (5 g/L) , high-dose AME group (10 g/L) , and high-dose AME + lipopolysaccharide (LPS) group ( 10 g/L AME + 1 mg/L TLR4 activator LPS) . Except for the control group , rats in all other groups were injected with bovine type Ⅱ collagen , Freund ’s complete adjuvant , and bleomycin to establish the RA-ILD model . The arthritis index and lung tissue wet-dry weight ratio of rats were tested . ELISA was applied to detect the levels of inflammatory factors interleukin (IL)-1β, IL-6 and tumor necrosis factor-α( TNF-α) in bronchoalveolar lavage fluid . Hematoxylin eosin staining was used to observe pathological changes of rat knee joint tissue and lung tissue . Western blot was applied to detect the expression of autophagy fac- tors Beclin 1 , microtubule-associated protein 1A/1B - light chain 3 (LC3) Ⅱ/ Ⅰ , and MyD88/TLR4/NF-κB p65 pathway related proteins in lung tissue . Results Compared with control group , knee joint tissue and lung tissue of rats in RA-ILD group were damaged , the arthritis index , lung tissue wet-dry weight ratio , levels of IL-1β, IL-6 , and TNF-α, the expression levels of MyD88 and TLR4 proteins , and p-NF-κB p65/NF-κB p65 ratio increased (P < 0. 01) , the expression of Beclin 1 and LC3 Ⅱ/ Ⅰ proteins decreased (P < 0. 01) . Compared with RA-ILD group , the low-dose and high-dose AME groups showed reduced tissue damage in rats , the arthritis index , lung tis- sue wet-dry weight ratio , levels of IL-1β, IL-6 , and TNF-α, the expression levels of MyD88 and TLR4 proteins , and p-NF-κB p65/NF-κB p65 ratio showed a dose-dependent decrease (P < 0. 05 or P < 0. 01), the expression of Beclin 1 and LC3 Ⅱ/ Ⅰ proteins showed a dose-dependent increase (P < 0. 05 or P < 0. 01) . Compared with high- dose AME group , the tissue damage of rats in the high-dose AME + LPS group was worsened , the arthritis index , lung tissue wet-dry weight ratio , levels of IL-1β, IL-6 , and TNF-α, the expression levels of MyD88 and TLR4 pro- teins , and p-NF-κB p65/NF-κB p65 ratio were higher (P < 0. 01), the expression of Beclin 1 and LC3 Ⅱ/ Ⅰ pro- teins was lower ( P < 0. 01) . Conclusion AME inhibits the MyD88/TLR4/NF-κB p65 pathway and alleviates lung injury in RA-ILD rats .

Exploring the mechanism of cistanche in the treatment of Alzheimer′sdisease based on network pharmacology and animal experiment

Zhao Jie1 , Huo Dongsheng2 , Zhu Hongbo1 , Zhang Shibin1 , Jia Jianxin2

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.015

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abstract:
To explore the mechanism of cistanche deserticola ( meat cistanche) in treating Alzheimer ′s disease (AD) through network pharmacology , molecular docking , and animal experiments . Methods Effective components of meat cistanche were mined from the TCMSP database , and AD-related targets were filtered using the SwissTargetPrediction , DisGeNET , and GeneCards databases . The intersection of these targets was analyzed using protein-protein interaction (PPI) networks . Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrich- ment analyses were conducted via the Metascape database . Molecular docking of meat cistanche ′s active compo- nents with core targets was performed using AutoDock Vina. Based on network pharmacology predictions , an AD model was established using 8-month-old SAMP8 mice , with Morris water maze tests assessing learning and cogni- tive functions , Nissl staining observing hippocampal neuron morphology , and enzyme-linked immunosorbent assays and Western blotting detecting the expression levels of cAMP signaling pathway-related proteins in hippocampal tis- sues . Results Network pharmacology analysis predicted that meat cistanche might act on 74 AD targets through 8 active components . Molecular docking showed high affinity of active components like acteoside with core targets such as ESR1 , BDNF , MAPK1 , and APP. KEGG analysis indicated involvement in pathways related to cancer , cAMP signaling , and AD . Animal experiments demonstrated that meat cistanche effectively improved learning and cognitive impairments in AD mice and alleviated hippocampal neuron damage . ELISA and Western blotting results indicated that meat cistanche significantly increased the expression levels of cAMP , PKA , P-CREB in the cAMP pathway and promoted the expression of downstream neurotrophic factor BDNF . Conclusion Meat cistanche can improve learning and cognitive disorders in AD model mice and may exert therapeutic effects on AD by up-regula- ting the cAMP signaling pathway and the expression of downstream BDNF protein targets , thereby improving hipp- ocampal neuron injury .

Breeding and genotype identification of CCR2 knockout mice

Zhang Huiru , Wang Anqi , Liu Chong , Zhou Yuanyuan , Xue Hui , Tu Jiajie

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.001

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The effect of lncRNA MALAT1/miR-15b-5p regulating the Wnt/β-catenin signaling pathway on lipopolysaccharide-induced chondrocyte inj ury

Zhao Zhi , Liu Mengkun , Zha Rifei , Zhang Tingbao , Wang Cheng

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.010

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abstract:
To explore the molecular mechanism of long non-coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 ( MALAT1) /microRNA-15b-5p ( miR-15b-5p) regulating the Wnt/β-catenin path- way in lipopolysaccharide (LPS)-induced chondrocyte injury in osteoarthritis . Methods ATDC5 cells were treated with 5 mg/L LPS to establish the osteoarthritis cell injury model , and the expression levels of MALAT1 and miR- 15b-5p in the cells were detected by RT-qPCR . The MTT , flow cytometry , Alizarin red staining , and ELISA were used to assess the effects of MALAT1 and miR-15b-5p on LPS-induced chondrocyte injury . The dual-luciferase re- porter gene assay was used to examine the regulatory relationship between MALAT1 and miR-15b-5p . Western blot assay was used to evaluate the expression of relevant proteins . Results In LPS-induced ATDC5 cells , MALAT1 expression decreased (P < 0. 05) . Compared to the control group , the LPS group exhibited reduced cell activity , an increased apoptosis rate , elevated levels of tumor necrosis factor-α, interleukin-6 , and interleukin-1β, a higher number of calcified nodules , increased expression levels of extracellular matrix degradation-related proteins MMP13 and ADAMTS5 , decreased expression levels of Collagen Ⅱ and Aggrecan , and increased protein expression levels of Wnt1 and β-catenin (P < 0. 05) . Overexpression of MALAT1 could mitigate the effects of LPS on chondrocyte activity , apoptosis , inflammatory response , osteogenic differentiation , extracellular matrix degradation , and the Wnt/β-catenin pathway (P < 0. 05) . Additionally , the overexpression of miR-15b-5p enhanced the impact of LPS on chondrocytes (P < 0. 05) . Conclusion MALAT1 is lowly expressed in LPS-induced chondrocytes , and it alle- viates LPS-induced chondrocyte injury by targeting miR-15b-5p to inhibit the Wnt/β-catenin pathway .

The role of P2X7R in cardiac remodeling

Yang Shasha1 , 2 , Mo Lihua1 , 2 , Wang Huibo1 , 2

DOI: 10.19405/j.cnki.issn1000-1492.2025.07.028

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