Acetylcholine Receptor Agonists Exert Cytoprotection Against Hypoxia/Reoxygenation Injury through Inhibiting Apoptosis and Promoting Mitochondrial Dynamics and Biogenesis

Activation of acetylcholine receptors (AChRs) exerted cardioprotection against ischemia/reperfusion (I/R) injury. However, the mechanisms underlying its are not fully understood. We investigated effects hypoxia/reoxygenation (H/R), condition that mimics an in vivo I/R, presence and absence AChRs agonists cardiomyoblast H9c2 cells. The cells (104 cells/well) were incubated hypoxic chamber with ischemic solution (30 min) followed by reoxygenation (120 normal media. activated either muscarinic (ACh, 10−6M) or nicotinic (GTS21, 10−9M) applied 5 min prior to hypoxia at onset reoxygenation. At end H/R protocols, cell viability, apoptosis, mitochondrial dynamics biogenesis determined. significantly decreased viability increased apoptosis fission (Drp1) compared control. Mitochondrial treated group was when Additionally, autophagic flux increasing level LC3II/I. ACh GTS21 via reduction autophagy before onset. fusion only hypoxia. Interestingly, Our findings demonstrated induced myocardial death biogenesis. cytoprotective In contrast, reducing These suggested predominantly through receptor activation.