小檗碱对急性缺血性脑卒中患者氧化应激及神经功能的影响

Effects of Berberine on Oxidative Stress and Neurological Function in Patients with Acute Ischemic Stroke

目的:探讨小檗碱对急性缺血性脑卒中患者血清丙二醛(MDA)、谷胱甘肽过氧化物酶(GSHPx)及神经功能的影响。方法:纳入110例急性缺血性脑卒中患者,随机分为治疗组55例和对照组55例。两组患者均给予西医常规治疗,治疗组在常规治疗同时加用盐酸小檗碱片口服,治疗周期为14 d。于治疗前及治疗7 d、14 d后检测患者的血清MDA、GSH-Px水平,并采用美国国立卫生研究院卒中量表(NIHSS)评价患者的神经功能缺损程度。结果:治疗7 d、14 d后,两组患者的NIHSS评分较治疗前均明显降低(P<0.05),且治疗组患者的评分低于对照组(P<0.05)。治疗7 d、14 d后,两组患者的血清MDA水平较治疗前均明显降低(P<0.05),GSH-Px水平较治疗前明显升高(P<0.05);且治疗组患者的血清MDA水平低于对照组(P<0.05),血清GSH-Px水平高于对照组(P<0.05)。结论:小檗碱能明显改善急性缺血性脑卒中患者的神经功能缺损程度,其作用机制可能与抑制机体的氧化应激反应有关。

Objective ： To explore the effects of berberine on the serum levels of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） and the neurological function in patients with acute ischemic stroke. Methods： One hundred and ten patients with acute ischemic stroke were selected and randomly divided into the treatment group （55 cases） and the control group （55 cases）. The patients in both groups were treated with routine therapy of western medicine and the patients in the treatment group were orally treated with berberine hydrochloride tablets in addition, with a course of 14 days. Before treatment and seven and fourteen days after treatment, the serum levels of MDA and GSH-Px were detected, and the neurological function was evaluated by National Institutes of Health Stroke Scale （NIHSS）. Results： Seven and fourteen days after treatment, the NIHSS scores of both groups were significantly decreased （ P 〈 0.05 ）, and the scores of the treatment group were lower than those of the control group （ P 〈 0.05 ）. Seven and fourteen days after treatment, the level of MDA in both groups was obviously decreased （ P 〈 0.05 ）, and the level of GSH-Px in both groups was obviously increased （ P 〈 0.05 ） ; the level of MDA in the treatment group was lower than that in the control group （ P 〈 0.05 ）, and the level of GSH-Px in the treatment group was higher than that in the control group （ P 〈 0.05 ）. Conclusion ： Berberine can significantly improve the degree of neurological deficit in patients with acute ischemic stroke, and its mechanism may be related to the inhibition of oxidative stress.