Effects of cell cycle inhibitor on astroglial proliferation and scar formation and neuroprotection after focal cerebral ischemia in rats

Objective To observe the effects of cell cycle inhibitor on astrocytic proliferation and scar formation and to study neuronal apoptosis after focal cerebral ischemia in rats.Methods Ischemic model was established by photochemistry method.T_2-weighted MRI was performed on the 3rd, 7th, and 30th day after focal cerebral ischemia.The expression of glial fibrillary acidic protein(GFAP)and apoptosis was observed by immunofluorescence.The protein levels of GFAP and proliferation cell nuclear antigen (PCNA), CyelinA and CyclinB1 were measured by Western blotting from the ischemic and sham animals finished on the 3rd, 7th, and 30th day.Results A marked and significant reduction of brain infarction volume was found in Olomoucine-treated ischemic animals(2.27%±0.28% , 1.87%±0.19%, 1.08%± 0.18%)as compared with controls(5.10%±0.35%, 4.60%±0.26%, 3.96%±0.28%, P0.05). Olomoucine significantly reduced the expression of GFAP, and Olomoucine could reduce scar formation on the 7th and 30th day in rats.On the 3rd day after focal cerebral ischemia, the TUNEL-positive staining number of control group(41±11)was higher than that of the treatment group(26±8, P0.05), and the apoptosis ratio of the treatment group(22.44%±2.17 %)was lower than that of control group(34.41%± 3.10%).Western blotting indicated that there were increased protein levels of control group for GFAP, PCNA, CyclinA and CyclinB1 compared to those of the treatment group on the 3rd, 7th and 30th day after cerebral ischemia.Conclusion Cell cycle inhibitor could partially inhibit activation and proliferation of astrocyte and neuronal apoptosis, decrease infarction volume after ischemia, and thereby further help create an environment that benefits neuronal survival and nervous function reconstruction.