摘要
目的观察赛庚啶的脑保护作用，并初步探讨其作用机制。方法采用Ｐｕｌｓｉｎｅｌｉ四动脉结扎法制作大鼠急性前脑缺血再灌注损伤的模型。结果缺血再灌注造成脑组织严重损伤，脑水分、脑钙及ＭＤＡ含量显著增高，脑组织ＬＤＨ含量明显减少，脑电图严重抑制，锥体细胞坏死。赛庚啶能剂量依赖性地逆转上述变化。结论赛庚啶具有明显的脑保护作用，其机制可能与其钙拮抗作用和抗氧化作用有关。
AIM This experiment was planned to study the cerebral protective effects of cyproheptadine and its mechanisms. METHODS Pulsinelli fourvessel occlusion method was used to make the cerebral ischemiareperfusion model. After 40 min ischemia and 1 h reperfusion, several indexes including LDH, MDA, brain calcium content (BCC) and brain water content (BWC) were tested. RESULTS BCC was increased from (173±79) μg·g-1 (brain dwt) to (209±201) μg·g-1 (brain dwt), accompanied by BWC, MDA content elevated while LDH decreased. Abnormal electroencephalography (EEG) and pathologic changes were also found. CPH 2 mg·kg-1 and 4 mg·kg-1 decreased the rising of BCC, reduced BWC, suppressed the elevation of MDA and LDH release in brain tissue, improved EEG and shortened the pathologic damages. CONCLUSION These results suggest that CPH can protect the brain tissue from ischemiareperfusion injury by reducing calcium accumulation, antilipid peroxide reaction and deleting free radicals.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1998年第2期160-162,共3页
Chinese Pharmacological Bulletin
关键词
脑缺血
再灌注损伤
药物疗法
赛庚啶
cyproheptadine
calcium antagonist
brain calcium
lipid peroxide
brain edema
lactate dehydrogenase
