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作 者:Hai-Chang Yin Wen-Zhu Zhuang Xin-Jie Jiang Di Liu
机构地区:[1]Postdoctoral Research Workstation,Heilongjiang Academy of Agricultural Sciences,Harbin 150069,China. [2]College of Life Science and Agriculture Forestry,Qiqihar University,Qiqihar 161006,China.
出 处:《Traditional Medicine Research》2024年第7期35-41,共7页TMR传统医学研究
基 金:National Natural Science Foundation of China(32202800);Natural Science Foundation of Heilongjiang Province(LH2022C104);Heilongjiang Province Education Department Fundamental Scientifc Research Funds(145109516);Qiqihar University Graduate Innovative Research Project(YJSCX2022016).
摘 要:Background: No other effects of atropine other than as an antagonist of muscarinic acetylcholine receptor (mAChR) have been found. Methods: In this study, human kidneyepithelial cells were treated with different physiological regulators. Results: Subsequently, it was found that atropine could significantly induce autophagy as demonstrated by the appearance of autophagosome-like double- or single-membrane vesicles in the cytoplasm ofhost cells and the number of GFP-LC3 dots. In addition, increased conversion of the autophagy marker protein LC3-I and LC3-II and increased p62/SQSTM1 indicatedincomplete autophagy. In addition, atropine induced autophagosome levels in a dose-dependent manner within a certain concentration range in human kidney epithelial cells. In atropine-treated mouse skeletal muscle cells containing nicotinic acetylcholinereceptors and rat cardiac muscle cells containing mAchR, atropine induced autophagy in mouse skeletal muscle cells but not in rat cardiac muscle cells. Furthermore, atropine did not induce autophagy in tissue cells containing mAchR in vivo but did in tissue cells not containing mAchR. Conclusion: This study expands the application and understanding of atropine’s action mechanism in the field of medicine.
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