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)-αwas 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-αwas 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.
ABSTRACT
Objective To investigate whether lipopolysaccharide (LPS) can induce vascular endothelial cell growth factor (VEGF) expression in microglia regulated by hypoxia inducible factor-1α(HIF-1α). Methods The cultured BV2 cells were divided into four groups:control group, LPS (100 μg/L) simulated group, LPS (100 μg/L)+LPS antagonist (LRS, 200 μg/L) intervened group and LPS (100 μg/L)+HIF-1αinhibitors FM19G11 (10 mmol/L) intervened group. Immunofluorescence staining, Western blotting and ELISA were used to detect the expressions of VEGF and HIF-1α. Results Compared with the control group, the VEGF expression level was obvious high in LPS simulated group (P<0.05). LRS inhibited this effect of LPS (P<0.05). The HIF-1αlevel was increased in LPS simulated group at 8 h post-injury (P<0.05). FM19G11, the inhibitor of HIF-1αreduced the expression of VEGF induced by LPS (P<0.05). Conclusion LPS can up-regulate the expression of VEGF by HIF-1α.