Plantamajoside alleviates hypoxia-reoxygenation injury through integrin-linked kinase/c-Src/Akt and the mitochondrial apoptosis signaling pathways in H9c2 myocardial cells

BMC Complementary Medicine and Therapies

Research

Fuming Liu¹  Qiang Wu¹  Yuying Du¹  Chao Cai¹  Fanying Gong¹  Jia Li¹  Guoliang Zhou²  Fang Liu³ 

[1] Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, 210029, Nanjing, China;The Chinese Medicine College, Nanjing University of Chinese Medicine, 210046, Nanjing, China;Xuzhou Hospital of Chinese Medicine, 221018, Xuzhou, China;

关键词: Hypoxia-reoxygenation injury;    Plantamajoside;    Network pharmacology;    ILK;    H9c2 myocardial cells;   

DOI  :  10.1186/s12906-023-03880-6

 received in 2022-11-29, accepted in 2023-02-10,  发布年份 2023

来源: Springer

【 摘 要 】

Myocardial ischemia–reperfusion injury(MIRI) is one of the common complications after myocardial infarction surgery, Oxidative stress is among the main mechanisms of myocardial ischemia–reperfusion injury. Plantamajoside (PMS), the main effective ingredient in the genus Plantain, has been reported to possess an antioxidation, anti-inflammatory and anti-apoptosis role. However, whether PMS can attenuate myocardial ischemia–reperfusion injury is not yet known. Herein, we explored the effects of PMS on hypoxia-reoxygenation (H/R) injury in H9c2 cardiomyocytes and the underling molecular mechanisms of the treatment. Network pharmacological analysis screened the top 31 key genes in the treatment of MIRI disease treated with PMS, and the result of molecular docking further illustrated the roles that the PMS play in the treatment of MIRI through its interference with integrin-linked kinase (ILK) target protein. PMS was not cytotoxic in the concentration range of 5–40 μM and increased cell survival after H/R injury in a concentration-dependent manner without affecting proliferation or growth. PMS significantly reduced the levels of lactate dehydrogenase, malonic dialdehyde, reactive oxygen species and cell apoptosis, and increased soperoxide dismutase activity compared with those of the H/R injury group. PMS promoted the protein and mRNA expression of ILK and Bcl-2, the protein expression of p-Akt, and reduced the protein and mRNA expression of Bax, Caspase-3, and Cytochrome c, the protein expression of p–c-Src. PMS has protective effects against H/R injury in H9c2 cells, and its protective mechanism may be related to reactive oxygen species clearance, activation of the ILK/c-Src/Akt pathway and inhibition of the mitochondrial apoptosis.

【 授权许可】

CC BY   
© The Author(s) 2023

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