Diabetes-associated liver injury becomes a dominant hepatopathy,leading to hepatic failure worldwide.The current study was designed to evaluate the ameliorative effects of ginsenoside Rh1(G-Rh1)on liver injury induced...Diabetes-associated liver injury becomes a dominant hepatopathy,leading to hepatic failure worldwide.The current study was designed to evaluate the ameliorative effects of ginsenoside Rh1(G-Rh1)on liver injury induced by T2DM.A T2DM model was established using C57BL/6 mice through feeding with HFD followed by injection with streptozotocin at 100 mg·kg^(−1).Then the mice were continuously administered with G-Rh1(5 and 10 mg·kg^(−1)),to explore the protective effects of G-Rh1 against liver injury.Results showed that G-Rh1 exerted significant effects on maintaining the levels of FBG and insulin,and ameliorated the increased levels of TG,TC and LDL-C induced by T2DM.Moreover,apoptosis in liver tissue was relieved by G-Rh1,according to histological analysis.Particularly,in diabetic mice,it was observed that not only the increased secretion of G6Pase and PEPCK in the gluconeogenesis pathway,but also inflammatory factors including NF-κB and NLRP3 were suppressed by G-Rh1 treatment.Furthermore,the underlying mechanisms by which G-Rh1 exhibited ameliorative effects was associated with its capacity to inhibit the activation of the Akt/FoxO1 signaling pathway induced by T2DM.Taken together,our preliminary study demonstrated the potential mechnism of G-Rh1 in protecting the liver against T2DM-induced damage.展开更多
基金supported by Jilin Science&Technology Development Plan(No.20200301037RQ).
文摘Diabetes-associated liver injury becomes a dominant hepatopathy,leading to hepatic failure worldwide.The current study was designed to evaluate the ameliorative effects of ginsenoside Rh1(G-Rh1)on liver injury induced by T2DM.A T2DM model was established using C57BL/6 mice through feeding with HFD followed by injection with streptozotocin at 100 mg·kg^(−1).Then the mice were continuously administered with G-Rh1(5 and 10 mg·kg^(−1)),to explore the protective effects of G-Rh1 against liver injury.Results showed that G-Rh1 exerted significant effects on maintaining the levels of FBG and insulin,and ameliorated the increased levels of TG,TC and LDL-C induced by T2DM.Moreover,apoptosis in liver tissue was relieved by G-Rh1,according to histological analysis.Particularly,in diabetic mice,it was observed that not only the increased secretion of G6Pase and PEPCK in the gluconeogenesis pathway,but also inflammatory factors including NF-κB and NLRP3 were suppressed by G-Rh1 treatment.Furthermore,the underlying mechanisms by which G-Rh1 exhibited ameliorative effects was associated with its capacity to inhibit the activation of the Akt/FoxO1 signaling pathway induced by T2DM.Taken together,our preliminary study demonstrated the potential mechnism of G-Rh1 in protecting the liver against T2DM-induced damage.
