| ObjectiveKidney in vivo by observing the side of the high-fat fed glucose in type 2 diabetic MKR mice transgenic blood glucose, blood insulin, renal function and renal cortex of IRS, PI-3K protein expression was observed in vitro hypoglycemic kidney Side of the high level of insulin in cultured human mesangial cells, IRS, PI-3K protein expression and insulin signaling pathway inhibitor resistance after use of pancreatic IRS, PI-3K protein expression, kidney hypoglycemic preliminary study Party control of insulin signaling pathway in diabetic nephropathy mesangial cells proliferation.Methods:1 Vivo:Select MKR mice 11 weeks of age 40, male and female, according to blood glucose and MKR mice were randomly divided into blank group, model group, treatment group, positive medicine control group. The basis of MKR mice fed with the control group, model group, treatment group and western medicine positive control group fed high fat diet, diet for 8 consecutive weeks, the mice were orally fed to 19 weeks of age began. Treatment group given glucose kidney side, the positive control group was given medicine appropriate level of sugar enalapril Gabay, gavage for 30 days; both model group and control group MKR mice were given distilled water for 30 days. Gavage once daily 17:00-18:00.30 days after the collection of specimens, fasting blood glucose, plasma insulin,24-hour urinary albumin,β2-microglobulin, BUN, Cr, renal cortex in the insulin receptor, phosphatidylinositol -3-- kinase. 2 In vitro:Human mesangial cells were studied, in vitro cell culture technology, according to different groups:A, normal group (HMC); B, model group (HMC+insulin); C, inhibitor group (HMC+insulin+LY294002) D Chinese medicine group (HMC+insulin+glucose kidney side solution) were added to different culture media, immunohistochemistry and Western Blotting detection of insulin receptor, phosphatidylinositol-3-- kinase protein expression. All the data are used SPSS 16.0 software for statistical analysis.Results:1 Vi vitro:Medicines MKR mice blood glucose, blood insulin levels,24-hour urinary albumin,β2-microglobulin, serum BUN, Cr were significantly lower than model group and western medicine group (P<0.01 or P<0.05); Medicines MKR mouse renal cortex of insulin receptor, phosphatidylinositol-3-- kinase protein expression level of model group and western medicine group was significantly lower, the difference was significant (P<0.01).2 In vitro:comparison with the normal group, model group, the insulin receptor, phosphatidylinositol -3-- kinase protein levels (P<0.05); with the model group, Chinese group and the insulin receptor inhibitor group phosphatidylinositol -3-- kinase protein levels decreased significantly (P <0.01); with the inhibitor group, the Medicines insulin receptor, phosphatidylinositol -3-- kinase protein expression was significant (P<0.05).Conclusion:1 High-fat fed glucose kidney side of the MKR mice have lower blood sugar, improve hyperinsulinemia, regulating protein metabolism and improve renal function and so on, can improve the renal hemodynamic abnormalities, lower glomerular filtration pressure and high Over the state, thereby inhibiting the accumulation of matrix proteins, reducing urinary protein leakage and delay the development of diabetic kidney injury.2 Kidney side to reduce high blood glucose insulin in cultured human mesangial cells in the insulin receptor, phosphatidylinositol -3-- kinase protein expression.3 Hypoglycemic diabetic kidney side to improve the mechanism of cell proliferation may interfere with insulin signaling pathway. Kidney side hypoglycemic insulin signaling pathway by inhibiting improve the cell proliferation and apoptosis, thereby reducing the glomerular mesangial cells (MCs) proliferation, MCs to reduce the secretion of extracellular matrix (ECM), reducing ECM accumulation, and thus play Reduce kidney damage and delay the occurrence of renal injury in diabetes, the role of development... |
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