出 处:《海军医学杂志》2017年第2期116-118,136,共4页Journal of Navy Medicine
摘 要:目的探讨地黄饮子对大鼠脑缺血再灌注损伤的保护作用。方法选取健康清洁级Wistar大鼠72只,雌雄不限,体质量260~280 g,随机分为A组、B组、模型组、正常组,每组18只。A组:在造模后每日灌服地黄饮子36 g/kg。B组:每日灌服尼莫地平12.5 mg/kg。模型组:造模后胃灌盐水1次/d。正常组:正常饮食。前3组造模:夹闭大鼠双侧颈总动脉,大鼠发生脑缺血再灌注损伤。灌药3周后检测脑组织内超氧化物歧化酶(SOD)、丙二醛(MDA)。Morris水迷宫实验和跳台实验比较大鼠学习记忆能力,测量大鼠脑梗死面积。结果模型组中SOD含量[(93.42±18.78)k U/g prot]明显低于正常组[(158.36±22.32)k U/g prot],MDA含量[(6.35±2.04)μmol/g prot]明显高于对照组[(2.63±1.86)μmol/g prot],差异有统计学意义(P<0.05),本实验造模成功。A组[(135.34±20.12)k U/g prot]和B组[(132.78±19.56)k U/g prot]的SOD含量明显高于模型组,MDA含量[A组:(3.46±1.75)μmol/g prot],B组:(3.82±1.82)μmol/g prot]明显低于模型组,差异有统计学意义(P<0.05)。A组和B组的学习能力和记忆能力的错误次数、潜伏期均明显少于模型组,A组和B组的潜伏期均明显少于模型组,差异有统计学意义(P<0.05)。A组和B组的脑梗死面积均明显小于模型组,且A组的脑梗死面积明显小于B组,差异有统计学意义(P<0.05)。结论地黄饮子能够改善受损的脑细胞血液循环减少梗死面积,改善大脑的能量代谢,改善被抑制的神经细胞,修复神经功能缺损,保护受损的神经元。Objective To explore the protective effects of rehmannia Yinzi on ischemic injury induced by reperfusion in rats. Methods Seventy-two clean-grade Wistar rats with a body weight of 260-280 g were randomly divided into 4 groups: group A , group B, the model group and the normal control group, each consisting of 18 animals. For the animals of group A , rehmannia Yinzi liquid was given by gavage at a dose of 36 g/kg following development of the model, and for animals of group B, nimodipine was given also by gavage at a dose of 12. 5 mg/kg. The animals of the model group received physiological saline by gavage following development of the model, and the animals of the control group received normal feed. In the animals of the former 3 groups, bilateral common carotid artery was clipped to develop the ischemia model, and then, blood reperfusion was performed to induce ischemic injury. Three weeks after ga-vage of rehmannia Yinzi, the levels of superoxide dismutase( SOD) and malondiadehyde( MDA) were detected in the brain tissue. Morris water maze experiment and platform-jump experiment were performed to detect the learning and memory capacity of the rats, and the ar-ea of infarction was measured as well. Results SOD level [ (93. 42 ± 18. 78) kU/g prot] in the model group was obviously lower than that of the normal control group [(158. 36 ±22. 32) kU/g prot],but MDA level [ (6. 35 ± 2. 04) jjimol/g prot] was significantly high-er than that of the control group, [ (2.63 ± 1.86) μmol/g prot] , and statistical significance could be noticed, when comparisons were made between the 2 groups( P 〈0. 05) . The animal model was successfully developed. The SOD levels of group A [( 135. 34 ± 20. 12) kU/g prot] and group B [(132. 78 ± 19. 56) kU/g prot] were significantly higher than those of the model group, and the MDA levels of group A [ (3.46 ±
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