Effects of pioglitazone on the expressions of glial fibrillary acidic protein and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats / 国际脑血管病杂志

ABSTRACT

Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groupssham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.