Neuroprotection of rifampicin in global cerebral ischemia via inhibiting microglial activation
10.3969/j.issn.1000-484X.2015.09.006
- VernacularTitle:利福平通过抑制小胶质细胞活化对大鼠全脑缺血发挥保护作用
- Author:
Beibei CHEN
;
Huimin CAO
;
Rong LI
;
Oumei CHENG
- Publication Type:Journal Article
- Keywords:
Rifampicin;
Global cerebral ischemia;
Microglia;
Inflammatory response
- From:
Chinese Journal of Immunology
2015;(9):1178-1182
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective effect of rifampicin in a rat model of global cerebral ischemia /reperfusion ( GCIR) and discuss the influence of rifampicin on microglial activation.Methods:The GCIR rat model was induced via the bilateral occlusion of the common carotid arteries and systemic hypotension.Forty-two male SD (Sprague-Dawley) rats were randomly assigned to three groups:sham group ,I/R and I/R+FRP treated group.The rats in I/R+RFP group were treated with rifampicin 20 mg/kg by intra-peritoneal injection 30 min after reperfusion , while the other groups were treated with normal saline.Morris water maze test was performed for neurobehavioral test ,HE staining was detected for pathomorphology changes of neurons in CA 1 region.Microglia was im-munohistochemically stained in CA 1 region using ionized calcium adaptive molecular 1 ( IBA-1) as the marker.The protein levels of IL-1β,IL-6 and TNF-αin the hippocampal tissues of rats were also measured by enzyme-linked immunosorbent assay.Results:Rifampin improved the behavior ,shorten the escape latency of rats following GCIR obviously ( P<0.05 ) and reduced the neuron damage in hipp-ocampal CA1 region of rats after GCIR (P<0.05).Additionally,in I/R+FRP treated group the activation of microglia also showed a significantly inhibited compared with I/R group(P<0.05).Futhermore,we also found the expression of IL-1β,IL-6 and TNF-αin hipp-ocampal reduced obviously in I/R+FRP group ( P<0.05 ).Conclusion: Rifampin have obvious protective effect in the rat model of GCIR.The underlying mechanism may be associated with inhibition the activation of microglia ,reduction the expression of IL-1β,IL-6 and TNF-αand suppression the inflammatory response finally.
