目的 :探讨黄芩苷对大鼠脑缺血再灌注自由基损伤的保护作用,为脑缺血再灌注损伤防治提供新的药物. 方法 :将大鼠随机分为假手术组、脑缺血再灌注组及黄芩苷治疗组.动物模型采用大脑中动脉缺血再灌注模型,用黄嘌呤氧化酶法和硫代巴比妥法分别测定脑组织缺血再灌注 3, 6 h时超氧化物歧化酶( SOD)和丙二醛的含量及黄芩苷对其的影响. 结果 :脑缺血 2 h再灌注后 3, 6 h时,脑组织 SOD分别为( 24.5 ± 0.28),( 16.27± 0.20) NU/mg,丙二醛分别为( 0.66± 0.32),( 1.62 ± 0.52) μ mol/g,与假手术组比较,脑组织 SOD明显降低( P< 0.01),丙二醛则明显增高( P< 0.01);黄芩苷治疗后脑组织 SOD分别为( 30.19± 0.36),( 25.74± 0.28) NU/mg,丙二醛分别为( 0.42± 0.26),( 0.78± 0.37) μ mol/g,与模型组相比,脑组织 SOD有所增高( P< 0.01),而丙二醛则有所降低( P< 0.01).并且,治疗组大鼠神经功能缺损评分较模型组增高( P< 0.05). 结论 :黄芩苷对脑缺血再灌注自由基损伤有一定保护作用.
AIM:To study the protective effects of baicalin against the impairments of free radical after cerebral ischemia reperfusion(IR),so as to provide new drug for the prevention and treatment of cerebral IR. METHODS:The rats were randomly divided into sham operated control group,IR group and baicalin treatment group.The cerebral IR models were established by middle cerebral artery occlusion(MCAO).The levels of superoxide dismutase(SOD) and malondiadehyde(MDA) were determined with xanthine oxidase method and thiobarbiturate 3 and 6 hours after IR,and the effects of baicalin on them were evaluated. RESULTS:Compared with the sham operated group,the levels of SOD in brain tissue were decreased[(24.56±0.28) and(16.27±0.20) NU/mg](P< 0.01),and the levels of MDA were decreased[(0.66±0.32) and(1.62±0.52) μmol/g](P< 0.01) significantly at 2 hour ischemia 3 and 6 hour reperfusion.After baicalic treatment,the SOD levels were increased[(30.19±0.36) and(25.74±0.28) NU/mg](P< 0.01),while those of MDA were increased[(0.42±0.26) and(0.78±0.37) μmol/g](P< 0.01) as compared with those in the model group.The scores of neurologic impairment in the treatment group were higher than those in the model group(P< 0.05). CONCLUSION:Baicalin has an protective effect against the impairment of free radical after local cerebral IR.
Chinese Journal of Clinical Rehabilitation