消旋四氢巴马汀对局灶性脑缺血-再灌注损伤模型大鼠的保护作用

Protective Effects of dl-Tetrahydropalmatine on Focal Cerebral Ischemia-reperfusion Injury in Rats

目的观察消旋四氢巴马汀(THP)对局灶性脑缺血-再灌注损伤大鼠的保护作用。方法用改良LONGA法制作大鼠局灶性脑缺血-再灌注损伤模型,缺血前15min腹腔注射THP10.0,5.0,2.5mg·kg-1,观察缺血3h再灌注3h后大鼠神经功能障碍、脑梗死范围、血清乳酸脱氢酶(LDH)和肌酸激酶(CK)含量,脑组织钙、水、丙二醛(MDA)和超氧化物歧化酶(SOD)含量,以及脑超微结构。结果THP能剂量依赖性降低神经功能行为评分,缩小脑梗死范围,抑制血清LDH、CK活力升高;THP10.0mg·kg-1可明显减轻脑水肿,减轻脑超微结构损害,提高脑组织SOD活性,降低MDA含量和脑组织钙聚集。结论THP对局灶性脑缺血-再灌注损伤模型大鼠有一定保护作用,其作用机制可能与抑制脑组织钙聚集、抗脂质过氧化反应有关。

Objective To study the protective effects of dl-tetrahydropalmatine （THP） on focal cerebral ischemiareperfusion injure in rats. Methods The modified LONGA method was used to make the model of focal cerebral ischemiareperfusion injury in rats. THP was ip injected at 10.0,5.0,2.5 mg · kg^-1 15 min before ischemia. The influence of THP were observed after ischemia for 3 h followed by reperfusion for 3 h on neurological deficits, size of cerebral infarction, lactate dehydrogenase （LDH） and creatine kinase （CK） activities in serum, contents of water, calcium, malondialdehyde （MDA） and superoxide dismutase （SOD） activity in brain tissue, and injure of brain uhrastructure in the model rats. Results THP dosedependently reduced neurological deficit scores, decreased the size of cerebral infarction and inhibited LDH and CK in serum. THP 10.0 mg · kg^-1 markedly lowered the water contents of injured brain, improved the damaged brain uhrastructure. THP also increased the activity of SOD, reduced the content of MDA and inhibited intracellular calcium accumulation in the cerebrum. Conclusion THP has protective effects against cerebral ischemia-reperfusion injury in rats, and mechanism of which might be related to inhibiting the lipid peroxides and reducing calcium accumulation.