title: Apigenin attenuates myocardial ischemia/reperfusion injury via the inactivation of p38 mitogen‑activated protein kinase.
abstract: Apigenin (Api) is a plant monomer associated with reducing the risk of heart disease. However, the mechanism of action remains to be fully elucidated. In the present study, it was hypothesized that API has cardioprotective effects by attenuating myocardial ischemia/reperfusion (I/R) injury. Rats were randomly subjected to sham operation, myocardial I/R alone or I/R + Api. Cardiac function was measured, and infarct size was evaluated by triphenyltetrazolium chloride staining following reperfusion. The myocardial enzyme leakage was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK). The myocardium was also assessed for total superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. The phosphorylation of p38 mitogen‑activated protein kinase (MAPK) was analyzed by western blotting. The present study reported for the first time, to the best of our knowledge, that I/R significantly increased infarct size, induced CK and LDH release, inhibited the activity of SOD and increased the levels of MDA, all of which were prevented by treatment with Api. In addition, I/R increased the phosphorylation of p38 MAPK, which was significantly decreased in the Api‑treated heart tissue samples following I/R, compared with the untreated heart tissue samples. In conclusion, the results of the present study demonstrated that Api inhibited the p38 MAPK signaling pathway to protect cardiomyocytes from I/R‑induced injury.
authors.affiliation: Department of Medical Affairs, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.
authors.forename: Xia
authors.initials: X
authors.lastname: Yang
authors.affiliation: Clinical Laboratory, Shaanxi Maternal and Child Care Service Centre, Xi'an, Shaanxi 710003, P.R. China.
authors.forename: Junlan
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Pharmacy, General Hospital of Lanzhou Command, PLA, Lanzhou, Gansu 730050, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Dermatology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Medical Affairs, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.
authors.forename: Xianjiao
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery, General Hospital of Lanzhou Command, PLA, Lanzhou, Gansu 730050, P.R. China.
authors.forename: Zilin
authors.initials: Z
authors.lastname: Li
mesh_terms: D000818:Animals; D047310:Apigenin / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000378:metabolism; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010766:Phosphorylation / Q000187:drug effects; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D047428:Protein Kinase Inhibitors; D008315:Malondialdehyde; D047310:Apigenin; D013482:Superoxide Dismutase; D048051:p38 Mitogen-Activated Protein Kinases; D003402:Creatine Kinase