The protective effect of Apelin-۱۳ against cardiac hypertrophy through activating the PI۳K-AKT-mTOR signaling pathway

  • سال انتشار: 1402
  • محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 26، شماره: 2
  • کد COI اختصاصی: JR_IJBMS-26-2_007
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 280
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نویسندگان

Yu Peng

Provincial Clinical Medical College of Fujian Medical University, Fuzhou ۳۵۰۰۰۱, Fujian, China

Ruan Jingming

Provincial Clinical Medical College of Fujian Medical University, Fuzhou ۳۵۰۰۰۱, Fujian, China

Chen Shaowen

Provincial Clinical Medical College of Fujian Medical University, Fuzhou ۳۵۰۰۰۱, Fujian, China

Huang Feng

Provincial Clinical Medical College of Fujian Medical University, Fuzhou ۳۵۰۰۰۱, Fujian, China

Zhu Pengli

Provincial Clinical Medical College of Fujian Medical University, Fuzhou ۳۵۰۰۰۱, Fujian, China

چکیده

Objective(s): To determine the protective effect of Apelin-۱۳ on cardiac hypertrophy through activating the PI۳K-AKT-mTOR signaling pathway.Materials and Methods: The phenylephrine-induced cardiomyocyte hypertrophy model was established in H۹C۲ cells in vitro. Electroporation transfection technology was utilized to prepare and screen the H۹C۲ cells inducing low expression of the angiotensin type one receptor-related protein (Si-APJ). H۹C۲ and Si-APJ cells were divided independently into five groups: the control group, the PE group, the PE+Apelin group, the PE+Rapa group, and the PE+Apelin+Rapa group. RT-PCR was performed to analyze the mRNA expression levels of myosin heavy chain ۷ (MYH۷). Expression of the PI۳K/AKT/mTOR pathway proteins and MYH۷ was investigated by western blot.Results: The expression of PI۳K/AKT/mTOR phosphorylated proteins was significantly higher in the PE group compared with the PE+Apelin group in H۹C۲ cells (P< ۰.۰۵). Conversely, in Si-APJ H۹C۲ cells, the expression of PI۳K/AKT/mTOR phosphorylated proteins was decreased (P< ۰.۰۵). In H۹C۲ cells, the expression of MYH۷ protein was increased in the PE group compared with the control group (P< ۰.۰۵). In the same cell line, the expression of MYH۷ in the PE+Apelin group was decreased significantly compared with the PE group (P< ۰.۰۵). In Si-APJ H۹C۲ cells, compared with the control group, the expression of MYH۷ in the PE group still increased significantly (P< ۰.۰۵). In contrast, in the same cell line, there was no statistically significant difference in MYH۷ expression between the PE+Apelin, PE+Rapa, and PE+Apelin+Rapa groups compared to the PE group (P> ۰.۰۵).Conclusion: Apelin-۱۳ reduces PE-induced cardiac hypertrophy by activating the PI۳K/AKT/mTOR signaling pathway.

کلیدواژه ها

Akt, Apelin-۱۳, Cardiac hypertrophy, mTOR, PI۳K

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