Yang Shaojun,Zhang Xuan,Lu Yanzhi,Wang Zhengqing.Protective effect of CR1-SCR1-3 protein on acute cerebral ischemia and reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1323-1326.
Yang Shaojun,Zhang Xuan,Lu Yanzhi,Wang Zhengqing.Protective effect of CR1-SCR1-3 protein on acute cerebral ischemia and reperfusion injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1323-1326.DOI:
Protective effect of CR1-SCR1-3 protein on acute cerebral ischemia and reperfusion injury in rats
Objective To investigate the effect of complements on acute cerebral ischemia and reperfusion (CI/R) injury and the protective effect of complement receptor 1 (CR1)-SCR1-3 protein. Methods A total of 75 adult male Sprague-Dawley rats were randomly divided into three groups including a sham operation group (
n
=15)
a CI/R injury group (
n
=30) and a CI/R injury +CR1-SCR1-3 group (
n
=30). Transient focal cerebral ischemia was induced by intraluminal middle cerebral arte
ry occlusion (MCAO) method. After MCAO for 1 h and reperfusion for 24 h
the effects of CR1-SCR1-3 protein on neurological deficits and cerebral infarct size were detected by neurofunctional deficit score and TTC staining
respectively. The activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in cerebral cortex were determined. The deposition of C4b in cerebral cortex and the pathological changes were also assessed. Results After CI/R injury for 24 h
CR1-SCR1-3 could significantly improve rat neurological functions (
P
0.05) and lead to a reduction in cerebral infarct size (P0.01). Pretreatment with CR1-SCR1-3 could decrease the MPO activity(
P
0.01) and the content of MDA(P0.05)
and increase the SOD activity in cerebral cortex (
P
0.01). Decreased C4b deposition as well as improved pathological changes were also observed in the CI/R injury+CR1-SCR1-3 group (
P
0.01). Conclusion Complement activation plays a critical role in CI/R injury
and CR1-SCR1-3 possesses a protective effect by inhibiting the over-activation of complement system.
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