格列本脲对急性一氧化碳中毒大鼠脑损伤保护作用的实验研究

发布时间：2018-05-02 21:24

本文选题：格列本脲 + 急性CO中毒　；参考：《兰州大学》2017年硕士论文

【摘要】：目的观察格列本脲对(Glibenclamide,GBC)对急性一氧化碳中毒大鼠脑损伤保护作用,并探讨其可能的作用机制。方法40只健康、雄性、S-D大鼠分为4组,分别是:A组(对照组),B组(中毒模型组),C组(DMSO组),D组(治疗组)。建立大鼠急性一氧化碳中毒模型,C组在中毒1h、6h、12h给予DMSO与盐水,D组在相同时间点给予格列本脲。分别于染毒2h、6h、12h、24h采血检测血清NSE、S-100β、TNF-α、IL-8,并在染毒24h后用爬行法测大鼠神经功能缺损评分,评分后处死大鼠比较脑病理形态学变化。结果(1)与对照组比较,其余染毒组血清NSE、S-100β蛋白水平在2h、6h、12h、24h均显著升高(P0.01);与模型组和DMSO组比较,治疗组NSE、S-100β蛋白水平在6h、12h、24h均显著降低(P0.01);B组与C组比较无明显差异(P0.05)。(2)与对照组比较,其余染毒组血清TNF-a及IL-8含量在2h、6h、12h、24h均显著升高(P0.01);与模型组和DMSO组比较,治疗组血清TNF-a及IL-8含量在6h、12h、24h均显著降低(P0.01);B组与C组比较无明显差异(P0.05)。(3)实验结束时,治疗组神经功能缺损评分较模型组及DMSO组显著降低(P0.01);B组与C组比较无明显差异(P0.05)。(4)病理形态学显示:模型组及DMSO组神经元变性、坏死、排列疏松紊乱、核固缩、尼氏体减少,治疗组脑损伤较模型组及DMSO组减轻。结论格列本脲可减轻急性CO中毒大鼠脑损伤,该作用可能与其抑制Sur1减轻脑细胞水肿、抑制炎症反应、抑制钙超载、抑制脑细胞凋亡有关。
[Abstract]:Objective to observe the protective effect of glibenclamide on brain injury in rats with acute carbon monoxide poisoning and to explore its possible mechanism. Methods Forty healthy male S-D rats were divided into 4 groups: control group A (control group), group B (DMSO group) and group D (treatment group). A rat model of acute carbon monoxide poisoning was established. Group C was given glibenclamide at the same time point as group D and group C were given glibenclamide at 1 h or 6 h or 12 h after acute carbon monoxide poisoning. The serum NSES-100 尾 -TNF- 伪 IL-8 was measured at 2 h, 6 h, 12 h and 24 h after exposure, and the neurological impairment score of rats was measured by crawling method after 24 h exposure. The rats were killed to compare the pathological changes of brain. Results (1) compared with the control group, the serum NSES-100 尾 protein level in the other groups increased significantly at 2 h, 6 h, 12 h and 24 h, compared with the model group and the DMSO group, the level of NSES-100 尾 protein in the treatment group decreased significantly at 6 h, 12 h and 24 h, and there was no significant difference between group B and group C in the level of NSES-100 尾 protein, compared with the control group (P 0.01, P 0.05, P 0.05, P 0.05, P 0. 05, P 0. 05, P 0. 05, P 0. 05, P 0. 05, P 0. 05, P 0. 05, P 0. 05. Compared with model group and DMSO group, the levels of serum TNF-a and IL-8 in the other groups increased significantly at 2 h, 6 h, 12 h and 24 h, respectively. Compared with the model group and the DMSO group, the serum TNF-a and IL-8 levels in the treatment group decreased significantly at 6 h, 12 h and 24 h, respectively. There was no significant difference between group B and group C at the end of the experiment. The neurologic impairment score of the treatment group was significantly lower than that of the model group and the DMSO group. There was no significant difference between group B and group C in the pathological morphology of neurons in the model group and DMSO group (P 0.05). The results showed that the neurons in the model group and the DMSO group were denatured, necrotized, disorganized, nuclear pyknosis and Nissl bodies decreased. The brain injury in the treatment group was less than that in the model group and DMSO group. Conclusion glibenclamide can attenuate the brain injury in rats with acute CO poisoning, which may be related to the inhibition of Sur1 on brain cell edema, inhibition of inflammatory reaction, inhibition of calcium overload and inhibition of apoptosis of brain cells.
【学位授予单位】：兰州大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R595.1

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