Apigenin inhibits pressure overload-induced cardiac hypertrophy

被引:0
|
作者
Dong, Xuan [1 ,3 ]
Zhou, Heng [2 ]
Zhang, Yan [2 ]
Xu, Man [2 ,3 ]
Hao, Yarong [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Geriatr, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
[2] Wuhan Univ, Renmin Hosp, Dept Cardiol, Wuhan, Hubei, Peoples R China
[3] Wuhan Univ, Cardiovasc Res Inst, Wuhan, Hubei, Peoples R China
关键词
Apigenin; cardiomyopathy; hypertrophic; cystic fibrosis; glycogen synthase kinase 3; oncogene protein v-akt; CANCER CELLS; HEART; TARGETS; REGULATORS; FIBROSIS; PATHWAY;
D O I
暂无
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
Apigenin (5,7,4'trihydroxyflavone), a nontoxic citrus flavonoid, possesses comprehensive bioactive properties including anti-oxidation, anti-inflammatory, anticancer and antivirus functions. However, little is known about the role of apigenin on cardiac hypertrophy and fibrosis. The objective of our present study was to investigate the effect of apigenin on cardiac hypertrophy induced by aortic banding (AB) in mice and to elucidate the underlying molecular mechanisms. The extend of cardiac hypertrophy was quantitated by two-dimensional and M-mode echocardiography as well as by pathology and gene expression of hypertrophic markers analyses of the heart specimen. Our data demonstrated that apigenin significantly attenuated cardiac hypertrophy induced by AB through inhibiting Akt/GSK3 beta pathway. Meanwhile, apigenin attenuated fibrosis and collagen synthesis. Taken together, these current findings indicated that apigenin, a feasible safe and natural treatment, has protective potential against cardiac hypertrophy.
引用
收藏
页码:3772 / 3778
页数:7
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