Icariin ameliorate diabetic myocardial hypertrophy by inhibiting autophagy via the AMPK/mTOR pathway
Objective: To observe the effect of Icariin on diabetic myocardial hypertrophy and explore its molecular mechanism. Methods: C57BL/6 mice were randomly divided into Ctrl group (normal control group), DM group (STZ intraperitoneal injection model), and DM+ICA group (diabetic C57BL/6 mice by intrag...
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Formato: | article |
Lenguaje: | EN |
Publicado: |
Editorial Board of Journal of Hainan Medical University
2021
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Materias: | |
Acceso en línea: | https://doaj.org/article/1dc3e47c37114bb2ad0889e65525a1a3 |
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Sumario: | Objective: To observe the effect of Icariin on diabetic myocardial hypertrophy and explore
its molecular mechanism. Methods: C57BL/6 mice were randomly divided into Ctrl group
(normal control group), DM group (STZ intraperitoneal injection model), and DM+ICA group
(diabetic C57BL/6 mice by intragastric Icariin solution 80mg/kg/d, for 3 consecutive weeks).
Real-time quantitative PCR was used to detect myocardial hypertrophy markers BNP and
β-MHC. Western blotting was used to detect myocardial AMPK, p-AMPK, mTOR, p-mTOR,
LC3B and Beclin1 protein expression. Echocardiogram was used to detect left ventricular mass
and ejection fraction. Results: Compared with the normal control group, the expression of
myocardial hypertrophy markers BNP and β-MHC mRNA in diabetic mice were significantly
increased; the expression of phosphorylated AMPK protein, autophagy-related protein LC3B
and Beclin1 were significantly increased, and the expression of phosphorylated mTOR
protein is significantly reduced; the left ventricular mass is significantly increased. The above
changes can be reversed after treatment with Icariin, but the effect of Icariin is blocked by the
autophagy inhibitor rapamycin. Conclusion: Icariin may inhibit autophagy and reduce diabetic
myocardial hypertrophy through AMPK-mTOR signaling pathway. |
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