The Effect Of PPAR-γ Pathways In T2DM Rats In Focal Cerebral Ischemia And The Intervention Of Procyanidins

To study the protection function and the mechanism of procyanidin from peroxidase hyperplasia factor activation receptor (ppar-gamma) path and endoplasmic reticulum stress through the establishment of type2diabetic rats focal cerebral ischemia model.90male SD rats were fed with high amounts of sugars and fats for4weeks, then the low-dose STZ (25.0mg·kg-1) was injected into caudal vein to make T2DM rat model.the rats in the model were divided into five groups randomly:Sham operation group(n=18), Control group(n=18),PC group(n=18), RSG group(n=18), and PC+GW9662group(n=18). The MCAO model was made after each group pretreated by drugs. Surgical procedures of sham operation group was the same as the above, but no thread inserted. Executing the rats24hours after cerebral ischemia, the neuroethology evaluations for each group of rats were made, and the cerebral pathological conformation were observed by HE staining, the expressions of PPAR-y, nuclear factor-kappa B(NF-κB), glucose-regulated protein78(GRP78) and C/EBP homologous protein (CHOP)detected by immunohistochemical and Western blotting, and the expressions of PPAR-y mRNA, NF-κB mRNA, GRP78mRNA and CHOP mRNA were detected by RT-PCR. The nerve function defect after cerebral ischemia improves obviously in PC and RSG group. compared with T2DM control group(P<0.01); There were no statistically significant differences in PC+GW9662group compared with control group(P>0.05); The PPAR-y and GRP78expression in PC and RSG group was higher than that in T2DM control group(P<0.05), however, the NF-κB and CHOP expression in PC and RSG group was lower than that in T2DM control group (P<0.05); PC+GW9662group showed opposite trend compared with RSG group.1, PC can improve T2DM focal cerebral ischemia in rats nerve cells form, making the cell boundaries clear and nucleoli are clear. At the same time neural function lack score can be reduced significantly in T2DM focal cerebral ischemia in rats.2, On the one hand, PC plays its anti-inflammatory effects to protect the brain cells of T2DM rats focal cerebral ischemia injury, that be related with the rising of ppar-gamma protein expression and the decresing of NF-κB protein expression through ppar-gamma pathway. On the other hand, PC can inhibit the endoplasmic reticulum stress occurs, maintain the steady state and reduce the endoplasmic reticulum cell apoptosis happen of T2DM rats focal cerebral ischemia through its antiapoptotic effect that be related with the improving of GRP78mRNA expression and to CHOP mRNA expression of suppression.3, ppar-gamma agonist RSG can be activated ppar-gamma pathways, play its anti-inflammatory effect, increase ppar-gamma mRNA expression and restrain NF-κB mRNA expression; GW9662as ppar-gamma antagonists, offset the neural protection PC effect, make ppar-gamma expression was reduced, NF-κB expression was increased, blocking access ppar-gamma for T2DM rats focal cerebral ischemia of protection.