Naringin mitigates myocardial strain and the inflammatory response in sepsis-induced myocardial dysfunction through regulation of PI3K/AKT/NF-κB pathway

Sepsis-induced myocardial dysfunction (SIMD) is a manifestation of severe sepsis and is the main cause of increased mortality in sepsis patients. Naringin (Nar) has been reported to possess various biological activities and pharmacological properties. Therefore, the present study was undertaken to evaluate whether Nar can protect rats from the effects of LPS-induced SIMD. SD Rats were pre-treated with Nar (50 and 100 mg/kg) for 7 days before administration of a single dose of LPS (10 mg/kg, i.p.) on the seventh day. We found that Nar treatment markedly improved the global strain and strain rate of longitudinal, circumference, and radial direction (GLS/GLSr, GCS/GCSr, GRS/GRSr) compared to the LPS group. The layer-specific strain decreased gradually from the endocardial layer to epicardial layer, and the most serious damage occurred in the endocardial layer. Moreover, Nar significantly decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and myocardial enzymes (CK, LDH, and AST) induced by LPS and attenuated the inflammation response. Finally, Nar also inhibited NF-κB nuclear translocation and the activity of iNOS in H9c2 cardiomyocytes by activating PI3K/AKT signaling pathway. These results suggest that naringin may possess novel therapeutic potential for protection against LPS-induced myocardial dysfunction.