Effects of rosuvastatin on neuronal apoptosis in cerebral ischemic stroke rats via Sirt1/NF-kappa B signaling pathway

OBJECTIVE: To investigate the effects of rosuvastatin on nerve cell apoptosis in rats with cerebral ischemic stroke through Sirt1/NF-kappa B pathway. MATERIALS AND METHODS: 30 model rats were divided into three groups: normal group. stroke group (rats with cerebral ischemic stroke) and stroke+RVT group (cerebral ischemic stroke rats treated with rosuvastatin). The expression of Sirt1/NF-kappa B, areas of stroke infarction, cell cycles, as well as apoptosis situation in different groups were detected by Western Blot, immunohistochemistry, histomorphological observation, triphenyl tetrazolium chloride (TTC) staining and flow cytometry as well as immunofluorescent staining. RESULTS: Optical microscope observation showed cells in normal group presented complete and clear cellular hierarchical structure, regular cell arrangement, bluish violet cell nucleus and pink cytoplasm. No damage or necrosis was observed under normal condition. In stroke group, the boundary line between cytoplasm and nucleus was blurry and some apoptosis bodies were also observed. However, after rosuvastatin treatment, necrosis disappeared in stroke+RVT group. Western Blot analysis showed that the expression of SIRT1 decreased and NF-kappa B elevated in stroke group compared with those in normal group (p<0.05). However, rosuvastatin could reverse the effects of stroke on SIRT1 and NF-kappa B (p<0.05). The results of immunohistochemistry and immunofluorescent staining also confirmed our findings in SIRT1 and NF-kappa B expression after stroke. The areas of cerebral infarction increased significantly in stroke group and this effect could also be reversed by rosuvastatin treatment (p<0.05). Besides, cell cycle detection also showed that rosuvastatin treatment could inhibit the shortening of G1. S as well as G2 periods in cell cycles after stoke (p<0.05). CONCLUSIONS: Rosuvastatin may have great effects on improving cerebral infarction condition in rats with cerebral ischemic stroke. The mechanisms may be through Sirt1/ NF-kappa B pathway, thereby reducing the apoptosis rate and improving cell cycle of brain cells.