Jichu yixue yu linchuang (Jun 2020)
miR-195 inhibitor reduces liver oxidative stress injury in type 1 diabetic mice
Abstract
Objective To investigate the effects of miR-195 on the expression of Sirt1 and its downstream oxidative stress and mitochondrial apoptosis-related proteins in the liver of type 1 diabetic C57BL/6 mice. Methods Mice were divided into control group (Control group), diabetes group (DM group), and miR-195 inhibitor group (DM+antago group). The DM group model was replicated according to the conventional method, and miR-195 inhibitor (2.5 mg/kg) was transfected into DM + antago group mice. The DM group and the control group were injected with scrambled shRNA (2.5 mg/kg) only as a control.Observe and record the increase and decrease of body weight and blood glucose of mice every week. Take fresh liver tissue, one part is processed and made by HE staining for histopathological observation; the part is used to determine the MDA content and T-SOD activity in liver tissue.RT-qPCR and Western blot were used to detect the mRNA and protein content of related indicators in the liver tissue of the three groups of mice. Results 1)Compared with the control group, the leaflets of the liver tissue in the DM group showed structural disorders, hepatocytes were significantly edema, and the cytoplasm was loose; compared with the DM group, the hematocyte edema in the DM+antago group was reduced. 2)Compared with the control group, miR-195 mRNA expression, MDA content and AcFoxo1/Foxo1 protein expression in the DM group were significantly increased (P<0.05), while Sirt1, Foxo1 mRNA and protein expression, and T-SOD activity were significantly reduced (P<0.05); Compared with the DM group, miR-195 mRNA expression, MDA content and AcFoxo1/Foxo1 protein expression in the DM + antago group decreased significantly (P<0.05), while Sirt1, Foxo1 mRNA and protein expression, and T-SOD activity were all Significantly increased (P<0.05). Conclusions The expression of miR-195 is increased in liver oxidative stress in type 1 diabetic rats. Sirt1 seems to be potential target of miR-195.