摘要
目的观察大鼠脑缺血再灌流损伤脑组织S-100β蛋白的变化规律;探讨肌苷对缺血性脑损伤的保护机制。方法成年SD大鼠建立大脑中动脉缺血(MCAO)再灌流模型,腹腔注射肌苷注射液,应用神经功能等级评分观察脑缺血再灌流后行为功能的恢复,免疫组化法检测脑缺血再灌流各时间点脑组织中S-100β的动态变化。结果对照组脑缺血再灌流后3d、7d、14d功能恢复、等级评分减低;缺血侧S-100β的免疫阳性反应于脑缺血再灌流后12h明显增强,随时间推移逐渐增强,3d达高峰,7d时有所下降,14d降至假手术组水平。治疗组治疗后神经功能评分在7—14d明显低于对照组,同时脑组织中S-100β蛋白表达水平较对照组显著升高。结论肌苷对缺血性脑损伤的功能恢复有一定的促进作用,其机制可能与增加脑组织中S-100β的表达有关。
Objective:To observe the expression and significance of S-100β in the cerebral tissue after reperfusion of focal cerebral ischemia , and to elucidate the mechanism of Inosine in hypoxia-ischemic brain damage. Method:The models of reperfusion of focal cerebral ischemia of SD rats were established by intraluminal middle cerebral artery occlusion (MCAO) with a nylon monofilament suture. Inosine was injected intraperitoneally twice before and 12h after reperfution. Neurological grade evaluation was applied to examine the behavioral recovery on these rats and immunohistochemical technique was used to investigate the dynamic changes of S-100β in cerebral tissue.Result:There was improvement in the score of neurologic grade in Inosine treatment group at 7d and 14d after reperfusion when compared with controlled group. In controlled group, the expression of S-100β increased from reperfusion 12h and peaked at 3d, then decreased to controlled group level at 14d. In treatment group, the neurologic grade scores decreased while the expression increased remarkablely at reperfusion 7-14d,when compared with controlled group.The use of Inosine could increase the expression of S-100β.Conclusion:It is suggested that Inosine could protect against hypoxia-ischemic brain damage, whose role might be reflected by increasing the expression of S-100β.Author′s address Qingdao People′s Hospital, Qingdao, 266001
出处
《中国康复医学杂志》
CAS
CSCD
2004年第3期191-193,共3页
Chinese Journal of Rehabilitation Medicine
基金
山东省自然科学基金和青岛市科技局资助项目(Y2001C04)