Diosgenin glucoside protects against myocardial injury in diabetic mice by inhibiting RIP140 signaling.

Abstract

, against myocardial injury in type 2 diabetic (db/db) mice and its molecular mechanism of action. Levels of serum and myocardial tissues, blood glucose and inflammatory cytokines, as well as cardiac function indicators, of db/db mice were measured, and DG's mechanism of action was evaluated by immunohistochemistry and Western blotting. We found that long-term DG treatment improved glucose tolerance and lipid profiles, reduced production of IL-1β, IL-6, and TNF-α, and decreased serum levels of the cardiac injury indicators creatine kinase and lactate dehydrogenase. Interestingly, DG also inhibited RIP140 signaling, which normally regulates transcription of estrogen receptor genes and influences expression of proinflammatory cytokines. Our study revealed a novel mechanism of DG's anti-inflammatory effect against myocardial injury via RIP140 signaling modulation in diabetic mice.