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Objective: To observe lipopolysaccharide (Lipopolysaccharide, LPS) induced infectious brain edema after activation of astrocytes, the law of apoptosis and the expression of iNOS and AQP4 astrocytes in infectious brain edema formation and development The role. Methods: 84 male Sprague-Dawley rats were randomly divided into 3 groups: control group (C group, n = 12); saline control group (S group, n = 12); edema group (L group, n = 60) . Edema group at 6 h after modeling, 12h, 24h, 48h, 72h divided into five subgroups (n = 12). Group C only separation of the left common carotid artery, left common carotid external carotid artery and left internal carotid artery, not injected lipopolysaccharide; S group to the left internal carotid artery injection of sterile saline 0.15ml; the L group left internal carotid artery injection LPS150μg (0.15 ml) rat model of infectious brain edema. HE staining, wet and dry weight, method of formamide, flow cytometry, PT-PCR and immunohistochemical staining were observed pathological changes of the brain tissue, brain water content, blood-brain barrier permeability, astrocyte cells of apoptosis, AQP4mRNA, GFAP, iNOS and AQP4 protein expression. Results: 1, brain tissue pathological changes: L rat brain diffuse edema formation; vertebral cell disorder, nerve cell degeneration and necrosis, inflammatory cell infiltration. Group C and S group, no significant changes in the cells arranged in neat rows. Brain water content and EB content: LPS lead to increased brain water content and EB content, 6h increased and reached the peak at 12h, 72h returned to normal. Brain water content and EB content was positively correlated (r = 0.767, P lt; 0.01) 3 the AQP4mRNA and protein: L group except the 72h group the remaining subgroups AQP4mRNA and protein expression was significantly higher (P lt; 0.05), 12h The highest expression, then decreased gradually. Group C and S groups was not statistically significant. AQP4mRNA and AQP4 protein expression was positive related (r = 0.991. The variation of P lt; 0.01); AQP4mRNA with brain tissue water content was being related (r = 0.739, P lt; 0.01); of AQP4 mRNA in EB content was being related (r = 0.930, P lt; 0.01). Astrocyte apoptosis rate and GFAP of iNOS protein expression: L group rat astrocyte cell body swelling hypertrophy processes increased extend, at each time point increased apoptosis rate (P lt; 0.05), 24h apoptosis most significant; GFAP, iNOS expression were increased In addition to 72h, 12h and reached the peak. Weak expression of various indicators of group C and group S, compared with no statistical significance (P gt; 0.05). Conclusion: 1, injection of lipopolysaccharide hindbrain tissue edema zone formation, cell degeneration; increased brain water content and EB content that lipopolysaccharide can damage the blood-brain barrier to cause infectious brain edema. 2, after the injection of lipopolysaccharide astrocyte morphology changes and GFAP expression increased the AQP4 and iNOS upregulation of AQP4 expression and brain tissue water content and EB content is positively correlated, indicating that lipopolysaccharide can cause astrocytes abnormal activation of the latter can induce the AQP4 and iNOS abnormal expression, promote the development of infectious brain edema formation. 3 after lipopolysaccharide injection, the increase in apoptosis in astrocytes, apoptosis peak later than astrocyte activation and iNOS expression peak, indicating that the the astrocyte activation mediated inflammatory response may promote cell apoptosis involved in the formation and development of infectious brain edema.
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