Experimental study on the role and mechanism of Allicin in ventricular remodeling through PPARα and PPARγ signaling pathways

• Autor(a) principal: LIU,Qiyun
• Data de Publicação: 2022
• Outros Autores: FU,Qian, DU,Jia, LIU,Xiaohui
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000102049
• topic: Allicin; PPARα; PPARγ signaling pathway; ventricular remodeling

Abstract The paper investigated the effects of Allicin on the changes of activities of PPARα and PPARγ signaling pathways, and the relations with the subsequent myocardial cell hypertrophy, apoptosis, myocardial interstitial remodeling, RAAS activation and heart failure. The heart obtained from the 1-day-old Wistar suckling rats was isolated and cultured in an ordinary medium. After adding AngII and AngII+ of different concentrations respectively, the conditions of cardiomyocyte hypertrophy, apoptosis and interstitial remodeling were observed. AngII activated the re-expression of β-MHC in cardiomyocytes, which increased the area of cardiomyocytes, indicating that myocardial hypertrophy had occurred, and the model of cardiomyocyte hypertrophy was successfully established. Compared with the control group, after being treated with different concentrations of Allicin for 24 h, the AngII-induced cardiomyocyte hypertrophy was significantly reversed, α-MHC expression increased, β-MHC expression decreased, and α/β-MHC ratio obviously increased. Allicin inhibited AngII-induced cardiomyocyte apoptosis, decreased Fas/FasL protein expression, increased Bcl-2 protein expression, and decreased Bax protein expression. The Bcl-2/Bax ratio increased significantly. PPARα and PPARγ signaling pathways are involved in the inhibition of cardiomyocyte hypertrophy. Allicin-activated PPARα and PPARγ pathways can reverse cardiomyocyte hypertrophy, inhibit cardiomyocyte apoptosis, and alter expressions of Bcl-2/Bax and Fas/Fas-L in apoptosis-related gene.