Ameliorative Effect Of Rehmannia Glutinosa Oligosaccharides On Insulin Resistance In Vitro And Its Mechanism

Objective:Rehmannia glutinosa Libosch. is a traditional Chinese medicinal drug and has been used for treatment of type 2 diabetes in China for thousands of years. This thesis is to study the ameliorative effect of Rehmannia glutinosa oligosaccharides (ROS) on insulin resistance, which is one of the key steps of pathophysiological mechanism in the natural history of type 2 diabetes, in cellular models induced by dexamethasone by means of pharmacological and molecular biological methods.Methods:3T3-L1 preadipocytes were cultured and the differentiation and proliferation of adipocytes were detected by MTT method. Insulin resistant 3T3-L1 adipocytes cell model was induced by dexamethasone and the change of glucose concentration in cell culture was determined after ROS treatment. The mRNA expressions of peroxisome proliferator-activated receptor gamma( PPAR-γ),adiponectin, ap2 and GLUT4 relating to the differentiation of adipocytes and insulin seneitivity as well as Resistin that can induce insulin resistance were detected by reverse transcription PCR(RT-PCR).Results:In the high glucose DMEM culture media, by means of MTT method, the absorbance at 570 nm of 3T3-L1 preadipocytes was increased and that of 3T3-L1 adipocytes was decreased. ROS(0.1³0 μg·ml^-1 )significantly increased glucose consumption in 3T3-L1 preadipocytes and adipocytes culture with a concentration-dependent effect. ROS enhanced the sensitivity of 3T3-L1 adipocytes to insulin and improved the insulin resistence of 3T3-L1 adipocytes induced by dexamethasone significantly. ROS(10 μg·ml^-1) can up-regulate mRNA expression of PPAR-γ, adiponectin, ap2 and GLUT4, inhibit that of Resistin.Conclusion:ROS can promote the proliferation of 3T3-L1 preadipocytes, inhibit the proliferation of 3T3-L1 adipocytes and significantly improve insulin resistance induced by dexamethasone. The roles of improving insulin resistence may related to the activation of PPAR-γ and regulation of related mRNA gene expressions of of adiponectin, ap2 and GLUT4, as well as inhibition of Resistin gene expression that can induce insulin resistence. The study primalarily illustrates the ameliorative effects of ROS on insulin resistance in vitro and its mechanism, demonstrates its values of potential clinical application for prevention and treatment of type 2 diabetes mellitus in the future.