Study on the role of ginkgetin in pressure overload-induced myocardial hypertrophy in mice
Journal Title: Journal of Air Force Medical University - Year 2023, Vol 44, Issue 8
Abstract
Objective To investigate the cardioprotective effect of ginkgetin ( GK) on pressure overload-induced myocardial hypertrophy in mice. Methods Pressure overload-induced myocardial hypertrophy was established by transverse aortic constriction (TAC) in mice. Twenty-four C57BL / 6J mice (8 weeks old) were randomly divided into TAC group (n = 8), TAC + GK group (n = 8) and Sham group (n = 8). The TAC group was not treated, the TAC + GK group was given GK every day after operation, and the Sham group experienced the same operation without 7 0 line tied. Echocardiography was used to evaluate the cardiac systolic function of mice. Echocardiography, the ratio of heart weight to tibial length, WGA staining, and the transcription level of Myh7 were applied to evaluate the degree of myocardial hypertrophy. The ratio of lung weight to body weight, serum brain natriuretic peptide (BNP) level, and the transcription level of Nppb were used to evaluate the degree of heart failure after operation. Finally, cardiac fibrosis was evaluated by Masson staining and the transcription level of fibrosis-related molecules. Results GK significantly improved the decrease of cardiac ejection fraction ( P < 0. 05) and fractional shortening ( P < 0. 01), decreased the thickness of interventricular septum (P < 0. 05) and left ventricular posterior wall ( P < 0. 05), reduced the ratio of heart weight to tibial length (P < 0. 05), and decreased the cross-sectional area of cardiomyocytes ( P < 0. 01 ) and the transcription level of hypertrophy-related gene Myh7 (P < 0. 01) in mice after TAC. GK significantly reduced the ratio of lung weight to body weight (P < 0. 05), decreased the content of BNP in serum (P < 0. 01), and also reduced the transcription level of Nppb in left ventricular myocardial tissue in mice after TAC (P < 0. 05). Finally, GK significantly reduced the degree of cardiac fibrosis in mice after TAC (P < 0. 01), and reduced the transcription levels of fibrosis-related molecules Tgfb1 (P < 0. 01), Col1a1 (P < 0. 05), and Col3a1 (P < 0. 05) in cardiac tissue of mice. Conclusion GK can improve cardiac function, reduce the degree of myocardial hypertrophy and heart failure, and alleviate myocardial fibrosis in mice after TAC.
Authors and Affiliations
SHI Guangyong, ZHANG Bing, ZHAO Lin, CHEN Yawu, JIN Zhenxiao, XU Xuezeng
Keywords
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