Abstract
Lipid metabolism disorder and inflammation are essential promoters in pathogenesis of liver injury in type 2 diabetes. Puerarin (PUR) has been reported to exert beneficial effects on many diabetic cardiovascular diseases and chemical-induced liver injuries, but its effects on diabetic liver injury and its mechanism are still unclear. The current study was designed to explore the therapeutic effect and mechanism of PUR on liver injury in a type 2 diabetic rat model induced by a high-fat diet combined with low-dose streptozotocin. The diabetic rats were treated with or without PUR (100 mg/kg/day) by gavaging for 8 weeks, and biochemical and histological changes in liver were examined. Results showed that treatment with PUR significantly attenuated hepatic steatosis by regulating blood glucose and ameliorating lipid metabolism disorder. Liver fibrosis was relieved by PUR treatment. PUR inhibited oxidative stress and inflammation which was associated with inactivation of NF-κB signaling, thereby blocking the upregulation of proinflammatory cytokines (IL-1β, TNF-α) and chemokine (MCP-1). This protection of PUR on diabetic liver injury is possibly related with inhibition on TGF-β/Smad signaling. In conclusion, the present study provides evidence that PUR attenuated type 2 diabetic liver injury by inhibiting NF-κB-driven liver inflammation and the TGF-β/Smad signaling pathway.
Highlights
Diabetes mellitus (DM) occupies a leading position in the morbidity and mortality statistics, especially in developed countries [1]
Apart from insulin resistance and hyperinsulinemia, lipid metabolism disorder in liver and subsequently increased oxidative stress accompanied with inflammation contribute to the progression of T2DM along with nonalcoholic fatty liver disease (NAFLD) and lead to fibrosis and potentially cirrhosis [6]
Throughout the 8-week administration, diabetic rats showed a significant decrease in body weight with increased food and water intake compared with normal rats
Summary
Diabetes mellitus (DM) occupies a leading position in the morbidity and mortality statistics, especially in developed countries [1]. Other than chronic macrovascular and microvascular complications, DM is associated with liverrelated mortality and has become an increasing risk of hepatocellular carcinoma [2]. Growing evidence suggests that patients with T2DM are at a high risk for nonalcoholic fatty liver disease (NAFLD) [3]. Diabetes is an independent risk factor for NAFLD progression, hepatocellular carcinoma development, and liver-related mortality [4]. The progressive lipid deposition and fibrosis in liver is the typical character of NAFLD [5]. Apart from insulin resistance and hyperinsulinemia, lipid metabolism disorder in liver and subsequently increased oxidative stress accompanied with inflammation contribute to the progression of T2DM along with NAFLD and lead to fibrosis and potentially cirrhosis [6]
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