Naringin attenuates rat myocardial ischemia/reperfusion injury via PI3K/Akt pathway-mediated inhibition of apoptosis, oxidative stress and autophagy
Autor: | Fengwei Li, Chuanbin Cao, Zhenjian Zhan, Neng Wang, Jin Qian, Wei Yao |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Cancer Research
PI3K/Akt autophagy naringin myocardial ischemia/reperfusion injury business.industry Autophagy apoptosis Inflammation General Medicine Articles Pharmacology medicine.disease_cause medicine.disease Immunology and Microbiology (miscellaneous) Apoptosis Medicine Phosphorylation oxidative stress medicine.symptom business Protein kinase B Reperfusion injury PI3K/AKT/mTOR pathway Oxidative stress |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-1015 1792-0981 |
Popis: | Naringin (NRG) has been reported to exert cardioprotective effects against multiple cardiovascular diseases, including lipopolysaccharide-induced and hyperglycemia-induced myocardial injury. However, the role of NRG in myocardial ischemia/reperfusion (I/R) injury remains unclear. In the present study, the PI3K/Akt pathway was investigated to evaluate the possible mechanisms underlying the roles of NRG in myocardial ischemia/reperfusion (I/R) injury. The levels of cardiac enzymes were measured by ELISA to evaluate the optimal dosage of NRG that could protect against myocardial I/R injury. Rats were administered 100 mg/kg of NRG and activities of myocardial enzymes, the level of cardiac apoptosis and inflammation, oxidant response, autophagy indicators and echocardiography were evaluated. The level of corresponding proteins was measured using western blotting. The results indicated that NRG elicited the best cardioprotective effects at a dose of 100 mg/kg by significantly reducing the levels of myocardial enzymes, apoptosis, inflammation, oxidative response and infarct size. Furthermore, NRG alleviated contractile dysfunction by increasing the left ventricular ejection fraction and fractional shortening. In addition, NRG markedly promoted the phosphorylation of Akt, while decreasing the level of autophagy indicator beclin-1 and the microtubule-associated protein 1B-light chain 3 (LC3B) II/ LC3BI ratio. However, PI3K/Akt inhibitor (LY294002) partially reduced the NRG induced phosphorylation of Akt and the reduction in beclin-1, along with the LC3BII/LC3BI ratio. The results of the present study demonstrated that NRG could attenuate myocardial I/R injury. |
Databáze: | OpenAIRE |
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