GLUT4 mediates the protective function of gastrodin against pressure overload-induced cardiac hypertrophy

被引:9
作者
Zhang, Miao [1 ]
Tan, Yanzhen [2 ]
Song, Yujie [2 ]
Zhu, Min [1 ]
Zhang, Bing [2 ]
Chen, Cheng [1 ]
Liu, Yingying [2 ]
Shi, Lei [2 ]
Cui, Jun [2 ]
Shan, Wenju [1 ]
Jia, Zipei [1 ]
Feng, Lele [2 ]
Cao, Guojie [1 ]
Yi, Wei [2 ]
Sun, Yang [1 ]
机构
[1] Fourth Mil Med Univ, Xijing Hosp, Dept Gen Med, Xian 710032, Peoples R China
[2] Fourth Mil Med Univ, Xijing Hosp, Dept Cardiovasc Surg, Xian 710032, Peoples R China
基金
中国国家自然科学基金;
关键词
Gastrodin; Cardiac hypertrophy; GLUT4; INJURY; LIVER;
D O I
10.1016/j.biopha.2023.114324
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Gastrodia elata exhibits extensive pharmacological activity; its extract gastrodin (GAS) has been used clinically to treat cardiovascular diseases. In the present study, we examined the effect of GAS in a mice model of pathological cardiac hypertrophy, which was induced using transverse aortic constriction (TAC). Male C57BL/6 J mice un-derwent either TAC or sham surgery. GAS was administered post-surgically for 6 weeks and significantly improved the deterioration of cardiac contractile function caused by pressure overload, cardiac hypertrophy, and fibrosis in mice. Treatment with GAS for 6 weeks upregulated myosin heavy chain alpha and down-regulated myosin heavy chain beta and atrial natriuretic peptide, while insulin increased the effects of GAS against cardiac hyper-trophy. In vitro studies showed that GAS could also protect phenylephrine-induced cardiomyocyte hypertrophy, and these effects were attenuated by BAY-876, and increased by insulin. Taken together, our results suggest that the anti-hypertrophic effect of gastrodin depends on its entry into cardiomyocytes through GLUT4.
引用
收藏
页数:10
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