The Experimental Study Of The Effect Of Complement Activation In The Rat Middle Cerebral Artery Occlusion Model

Object: The pathophysilogical mechanism of cerebral ischemia injury is very complicated. Recent research demonstrate that conplement activation is invovled in the pathophysilogical process of perihematom tissue injury in cerebral hemorrhage. But the effect of complement activation in cerebral ischemia is still uncertain. The aim of the study is to investigate the relationship between the expression of complement C1q and C3d protein and the change of brain water content, the permeability of BBB, pathological alteration of brain tissue in rat after MCAO. And observe the effect of complement deplection with CVF. We try to explore the action of complement activation in cerebral ischemia reperfusion injury and explore a new way for clinical neuroprotective therapy.Method: Along with the application of intra-luminal technology, fishing-line (0.23mm in diameter) were used to create the focal cerebral ischemia reperfusion model in healthy Sprague-Dawley rat, extract the line after occlusion 2h. We estimate the markers such as the expression intensity of complement C1q and C3d protein, brain water content, the permeability of BBB, the alteration of pathology and ultra-structure of cerebral ischemical tissue at different time before and after MCAO, observe the change of previou markers in the group of depleting complement with CVF, and analysis the relationship between them. Result:1．The expression of complement C1q and complement C3d protein is not observed in normal brain tissue.2．The positive expression of complement C1q and C3d protein appear at 6h after MCAO, reach the peak at 72h, decrease gradually after then, the expression is still higher than normal tissue at 120h.3．Complement resides in cytoplasm of the glia cell and nerve cell in cortical and basal ganglia of ischemic area after cerebral ischemia reperfusion injury.4．The expression intensity of complementC1q and C3d after MCAO and the raise of brain water content and permeability of BBB after MCAO is parallel.5．CVF can significantly inhibit the expression of complement C1q and C3d, reduce brain infarct volume, alleviate brain water content, depress the permeability of BBB, lighten the damage of in pathology and ultra-structure of brain tissue. Conclusion: The experimental results suggested complement activation was involved in the pathophysilogical process of cerebral damage after cerebral ischemia. CVF deplete complement can alleviate brain edema, reduce infarct volume, depress the permeability of BBB, lighten the damage of brain tissue. It processes neuroprotective strategy.