Ginsenoside-Mc1 reduces ischemia/reperfusion-induced cardiac arrhythmias through activating JAK2/STAT3 pathway and attenuating oxidative/endoplasmic reticulum stress in hyperlipidemic rats

Abstract Objectives Patients suffering from myocardial ischemia-reperfusion (IR) injuries usually have varying degrees of negatively-affecting comorbidities like hyperlipidemia. We evaluated the preconditioning effect ginsenoside-Mc1 on reperfusion injury-induced arrhythmias, along with cardiac oxidative stress, endoplasmic reticulum stress protein expression, and histological damage in hyperlipidemic rats, further, explore role JAK2/STAT3 activity. Methods Thirty-five Sprague–Dawley rats fed a high-fat diet for eight weeks. Ginsenoside-Mc1 (10 mg/dL, IP) was administered to daily one month before IR injury. injury induced by 35 min LAD coronary artery ligation subsequent 60-min reperfusion. A selective JAK2 inhibitor (AG490) injected Electrocardiography recorded arrhythmias (ventricular premature complexes, tachycardia, fibrillation) were phase according Lambeth convention. Hematoxylin-Eosin staining, spectrophotometry, Western blotting techniques employed measure endpoints. Results significantly increased reperfusion-induced counts, timing, incidence, severity. The expression proteins (p-PERK, p-eIF2?, CHOP), marker malondialdehyde upregulated following induction, whereas antioxidant superoxide-dismutase reduced, as compared untreated-hyperlipidemic rats. Administration corrected arrhythmogenic feature injury, reduced phosphorylation PERK, eIF2?, CHOP, improved changes. Interestingly, inhibition pathway via AG490 abolished ginsenoside-Mc1-induced cardioprotection. Conclusions Taken together, exerts substantial anti-arrhythmogenic influences against through activation reduction oxidative/endoplasmic stress.