Naringenin Attenuates Myocardial Ischemia-Reperfusion Injury via cGMP-PKGIα Signaling and In Vivo and In Vitro Studies.

摘要: Endoplasmic reticulum (ER) stress and oxidative contribute greatly to myocardial ischemia-reperfusion (MI/R) injury. Naringenin, a flavonoid derived from the citrus genus, exerts cardioprotective effects. However, effects of naringenin on ER as well under MI/R condition detailed mechanisms remain poorly defined. This study investigated protective effect MI/R-injured heart with focus cyclic guanosine monophosphate- (cGMP-) dependent protein kinase (PKG) signaling. Sprague-Dawley rats were treated (50 mg/kg/d) subjected surgery or without KT5823 (2 mg/kg, selective inhibitor PKG) cotreatment. Cellular experiment was conducted H9c2 cardiomyoblasts simulated treatment. Before treatment, cells incubated (80 μmol/L). PKGIα siRNA employed inhibit PKG Our in vivo vitro data showed that effectively improved function while it attenuated apoptosis infarction. Furthermore, pretreatment suppressed MI/R-induced evidenced by decreased superoxide generation, MDA level, gp91phox expression, phosphorylation PERK, IRE1α, EIF2α reduced ATF6 CHOP. Importantly, significantly activated cGMP-PKGIα signaling inhibition (in vivo) vitro) not only abolished these actions but also blunted naringenin’s inhibitory against stress. In summary, our demonstrates treatment protects injury reducing via Its deserves further clinical study.