Asiatic acid alleviates Ang-II induced cardiac hypertrophy and fibrosis via miR-126/PIK3R2 signaling
| Autor: | Yongjuan Ruan, Junhui Xing, Haiyu Li, Xiaoxu Tian, Zhe Meng |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty RC620-627 Angiogenesis Endocrinology Diabetes and Metabolism Medicine (miscellaneous) 030204 cardiovascular system & hematology Muscle hypertrophy 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Fibrosis Internal medicine PI3K/Akt signaling pathway medicine TX341-641 Nutritional diseases. Deficiency diseases Pathological PI3K/AKT/mTOR pathway Nutrition and Dietetics Nutrition. Foods and food supply Akt/PKB signaling pathway business.industry Research PIK3R2 miR-126 medicine.disease In vitro Cardiac hypertrophy 030104 developmental biology Endocrinology cardiovascular system business |
| Zdroj: | Nutrition & Metabolism Nutrition & Metabolism, Vol 18, Iss 1, Pp 1-8 (2021) |
| ISSN: | 1743-7075 |
| DOI: | 10.1186/s12986-021-00596-7 |
| Popis: | Background Cardiac hypertrophy is an independent risk factor of many cardiovascular diseases. Studies have demonstrated that microRNA-126 (miR-126) was involved in angiogenesis during physiological and pathological process. However, its role in cardiac hypertrophy has not been known clearly. Our previous study demonstrated that asiatic acid (AA) has obvious protective effect on cardiac hypertrophy. Here, this study aimed to discover the regulatory role of miR-126 and its mechanism in cardiac hypertrophy, and to determine whether AA’s anti-hypertrophy effect is partially miR-126 dependent. Methods Male Sprague Dawley rats were AngII infused via osmotic minipumps for 4 weeks and were treated with AA (20 mg/kg/day) by oral gavage. Cardiac hypertrophy was assessed using the echocardiography and histological analysis. In vitro studies,cardiomyocyte and cardiac fibroblasts (CF) were treted with AngII and AngII plus AA. And, the effect of AA on miR-126 and PI3K/AKT signaling pathway was investigated. Results Treatment of rats with AA decreased the ratio of heart weight to tibia length and hypertrophy markers. In vitro exprements demonstrated that AA significantly attenuated AngII-induced cardiac growth and cardiac fibroblast collagen expression. Moreover, our results found downregulation of miR-126 and activation of PI3K/AKT signaling pathway in AngII infusion induced cardiac hypertrophy model. It was also determined that miR-126 targets PIK3R2 directly. Conclusions AA supplementation upregulated the expression of miR-126 and conferred cardio-protection effect against AngII induced cardiac hypertrophy. |
| Databáze: | OpenAIRE |
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