Salidroside-regulated Glucose Metabolism with Down-regulation of Micro RNA-370 in Type 2 Diabetic Mice / 医药导报

ABSTRACT

Objective To observe the effects of salidroside regulating glucose metabolism in type 2 diabetic mice,then to explore the molecular mechanism. Methods Type 2 diabetes model was induced by feeding high-fat diet and intraperitoneal injecting STZ to male C56BL/6J mice,then the glucose related indexes,micro RNA-370 levels in the serum and liver tissue and the expression of gluconeogenesis key protein(G6Pase and PEPCK) in the liver tissue to observe the treatment effects of salidro-side on type 2 diabetic-caused gluose metabolic disorder.In cell test,we isolated primary hepatocytes,then silenced or over-ex-pressed micro RNA-370 in mouse primary hepatocytes to observe the molecular mechanism of glucose metabolic regulation of the micro RNA-370 and salidroside. Results Treated with salidroside 40,80 and 160 mg·kg-1,the results showed that compared with the model control group,the glucose related indexes were all improved significantly.The relative expression levels of micro RNA-370 in serum and liver,and that of PEPCK and G6Pase all reduced in different degrees,dose-dependently.The changes of middle and high dose group decreased significantly(P<0.05),that of low dose group had a decreasing trend but no statistically significant.In the cell test,compared with the normal control group,salidroside alone group and micro RNA-370 inhibitor group were able to reduce the protein expression level of PEPCK and G6Pase(P<0.05),micro RNA-370mimic alone group can signifi-cantly increase the protein expression level of PEPCK and G6Pase(P<0.05),compared with the micro RNA-370mimic alone group,combining micro RNA-370 mimic and salidroside can significantly reverse the increasing caused by micro RNA-370 mimic alone(P<0.05). Conclusion Our research found that salidroside can improve glucose metabolism disorder in type 2 diabetic mice,and at least in part,through the suppression of micro RNA-370 expression for the first time.