摘要
目的:通过检测脑组织内丙二醛(MDA)、超氧化物歧化酶(SOD)含量和谷胱甘肽过氧化物酶(GSH-Px)活性,探讨亚低温、川芎嗪对缺氧缺血性脑病幼鼠的脑保护作用。方法:将142只大鼠幼鼠随机分为常温缺血组(A组)、常温缺血+亚低温组(B组)、常温缺血+川芎嗪组(C组)、常温缺血+亚低温+川芎嗪组(D组),建立缺氧缺血性脑病幼鼠模型,各组给予相应的治疗,检测各组幼鼠脑组织内MDA、SOD含量及GSH-Px活性,对结果进行比较和统计分析。结果:B组、C组、D组幼鼠MDA含量均较A组低,SOD含量及GSH-Px活性高于A组,提示亚低温和川芎嗪治疗缺氧缺血性脑病有效;D组脑组织内MDA含量较B组、C组低,SOD含量、GSH-Px活性较B组、C组高,差异有统计学意义(P均<0.01)。B、C两组MDA和SOD含量及GSH-Px活性比较差异无统计学意义(P>0.05)。结论:亚低温、川芎嗪均能减轻缺氧缺血引起的脑损伤,二者联用疗效更佳。
Objective：To research the cerebral protective effects of mild hypothermia and ligustrazine by detecting the MDA, SOD levels and GSH-Px activity of brain tissues in young rats with hypoxic ischemic encephalopathy. Methods： Totally 142 young rats were randomly divided into four groups, group A, ormal temperature and ischemia; group B, normal temperature and mild hypothermia; group C, normal temperature, ischemia and ligustrazine; group D, normal temperature, ischemia, mild hypothermia and ligustrazine. Establish rat models of hypoxic-ischemic encephalopathy, give each group appropriate treatment, and detect the MDA, SOD levels and GSH-Px activity of brain tissues, then compare and statistical analyze the results. Results： The MDA levels of group B, C and D were lower than that of group A, and the SOD levels and GSH-Px activity of these groups were higher than those of group A, what meant the treatments of group A were effective. The MDA＇level of group D was lower than that of group B and C, and the SOD level and GSH-Px activity were higher; there were statistically significant differences （ all P〈0.05 ）. In group B and C, there were no statistically significant differences on MDA, SOD levels and GSH-Px activity （P〉0.05）. Conclusions： Mild hypothermia and ligustrazine can reduce brain damage caused by hypoxic ischemic. It may improve the efficacy when both treatments were used in combination.
出处
《儿科药学杂志》
CAS
2013年第9期3-5,共3页
Journal of Pediatric Pharmacy
关键词
亚低温
川芎嗪
缺氧缺血性脑病
丙二醛
超氧化物歧化酶
谷胱甘肽过氧化物酶
Mild hypothermia
Ligustrazine
Hypoxic ischemic encephalopathy
Malondialdehyde
Superoxide dismutase
Glutathione peroxidase
