Abstract: Abstract: Objective To observe the effects of atorvastatin on the microglia activation after traumatic brain injury (TBI). Methods Sixty adult male C57/BL6 mice were randomly divided into sham group, atorvastatin group and saline group, 20 mice for each group. The atorvastatin group and saline group were given hydraulic combat to establish TBI mouse model. The shame group underwent the same surgical procedure without being exposed to percussion injury. The atorvastatin group was treated with atorvastatin (orally, 1 mg/kg)1 h after TBI and for 7 consecutive days. The saline group was given sa⁃ line orally. The expression of microglia (Iba-1+ ) at the 1st, 3rd, and 7th day after TBI and matrix metalloproteinase -9 (MMP- 9) around the lesion at the 3rd day after TBI were detected by immunohistochemical staining. Tumor necrosis factor (TNF)-α was detected by Western blot assay at the 3rd day after TBI. Results The positive expression of Iba-1+ microglia was signifi⁃ cantly decreased in atorvastatin group than that of saline group at the 1st, 3rd, and 7th day after TBI (80.00±7.44 vs. 118.40± 6.65， 85.60±10.87 vs. 189.00±7.51， 69.40±5.54 vs. 102.40±10.89, P＜0.05). The positive expression of MMP-9 was signifi⁃ cantly decreased in atorvastatin group compared with that of saline group at the 3rd day after TBI (86.80±8.40 vs. 133.80± 8.46, P＜0.05). Results of Western blot assay showed that the positive expression of TNF-α was significantly decreased in astorvastatin group than that of saline group at the 3rd day after TBI (0.64±0.01 vs. 0.97±0.02， P＜0.05). Conclusion Ator⁃ vastatin can reduce inflammation factor by influencing the microglia activation after TBI in mice.

Key words: craniocerebral trauma, microglia, matrix metalloproteinase 9, tumor necrosis factor-alpha, Atorvastatin