Polydatin exhibits the hepatoprotective effects through PPAR-α/-β signaling pathway in Streptozocin-induced diabetic mice

Polydatin has a wide range of pharmacological activities, yet the underlying effects on diabetic hepatopathy remain unclear. Diabetic model was established by feeding mice a high-energy diet for 4 weeks combined with streptozotocin, then hepatopathy model was confirmed by histopathological observation after another 4 weeks. Polydatin supplementation (50 or 100 mg/kg/day, i.g.) for an additional 4 weeks improved signs of liver damage compared to untreated mice. The protein and mRNA expressions of PPARs were down-regulated, while of NF-κB, iNOS and COX-2 were up-regulated following diabetic hepatic injury, and TNF-α and IL-1β were increased in serum. Polydatin supplementation up-regulated PPAR-β expression, but elevated PPAR-α only at 100 mg/kg/day, while had no influence on PPAR-γ. Polydatin also corrected the above abnormal proinflammatory cytokines levels. In conclusion, polydatin can improve hepatic injury in diabetic mice, which may be due to a reduction of proinflammatory cytokines through the promoted expressions of PPAR-β and -α.