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학술저널
저자정보
Zhao Junxiong (Department of Pharmacy The Second Affiliated Hospital Hengyang Medical School University of South C) Wu Qian (Department of General Practice The Second Affiliated Hospital Hengyang Medical School University of) Yang Ting (Department of Pharmacy The Second Affiliated Hospital Hengyang Medical School University of South C) Nie Liangui (Department of Cardiology The First Affiliated Hospital Hengyang Medical School University of South) Liu Shengquan (Department of Cardiology The First Affiliated Hospital Hengyang Medical School University of South) Zhou Jia (Department of Ultrasound Medicine The First Affiliated Hospital Hengyang Medical School University) Chen Jian (Department of Critical Care Medicine The Affiliated Nanhua Hospital Hengyang Medical School Univers) Jiang Zhentao (Department of Cardiology The Affiliated Nanhua Hospital Hengyang Medical School University of South) Xiao Ting (Department of Cardiology Shenzhen Longhua District Central Hospital Longhua Central Hospital Affili) Yang Jun (Department of Cardiology The First Affiliated Hospital Hengyang Medical School University of South) Chu Chun (Department of Pharmacy The Second Affiliated Hospital Hengyang Medical School University of South C)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제6호
발행연도
2022.11
수록면
541 - 556 (16page)
DOI
10.4196/kjpp.2022.26.6.541

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Myocardial fibrosis is a key link in the occurrence and development of diabetic cardiomyopathy. Its etiology is complex, and the effect of drugs is not good. Cardiomyocyte apoptosis is an important cause of myocardial fibrosis. The purpose of this study was to investigate the effect of gaseous signal molecule sulfur dioxide (SO2) on diabetic myocardial fibrosis and its internal regulatory mechanism. Masson and TUNEL staining, Western-blot, transmission electron microscopy, RT-qPCR, immunofluorescence staining, and flow cytometry were used in the study, and the interstitial collagen deposition, autophagy, apoptosis, and changes in phosphatidylinositol 3-kinase (PI3K)/AKT pathways were evaluated from in vivo and in vitro experiments. The results showed that diabetic myocardial fibrosis was accompanied by cardiomyocyte apoptosis and down-regulation of endogenous SO2-producing enzyme aspartate aminotransferase (AAT)1/2. However, exogenous SO2 donors could up-regulate AAT1/2, reduce apoptosis of cardiomyocytes induced by diabetic rats or high glucose, inhibit phosphorylation of PI3K/AKT protein, up-regulate autophagy, and reduce interstitial collagen deposition. In conclusion, the results of this study suggest that the gaseous signal molecule SO2 can inhibit the PI3K/AKT pathway to promote cytoprotective autophagy and inhibit cardiomyocyte apoptosis to improve myocardial fibrosis in diabetic rats. The results of this study are expected to provide new targets and intervention strategies for the prevention and treatment of diabetic cardiomyopathy.

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