七氟醚后处理对大鼠脑缺血再灌注时氧化应激和炎症反应的影响
发布时间：2018-11-03 08:20
【摘要】：目的:评价七氟醚后处理对大鼠脑缺血再灌注时氧化应激及炎症反应的影响,以探讨其脑保护的作用机制。方法:雄性清洁级健康SD大鼠36只,体重220~260 g,12~14周龄,采用随机数字表法分为3组:假手术组(Sham组)、脑缺血再灌注组(I/R组)和脑缺血再灌注+七氟醚后处理组(SPC组),每组12只。I/R组和SPC组采用线栓法建立脑缺血再灌注损伤模型,缺血30 min,再灌注24 h;Sham组大鼠不阻塞大脑中动脉。SPC组于再灌注即刻给予吸入2.6%的七氟醚15 min。于再灌注24 h末采用Longa法进行神经行为学评分,处死各组大鼠,取脑组织,采用TTC法染色测定脑组织的梗死面积、Western blot法检测Iba-1和HO-1蛋白表达水平,测定脑组织ROS、SOD、MDA、TNF-α和IL-1β的水平。结果:(1)与Sham组比较,I/R组和SPC组神经行为学评分升高,脑梗死面积增加(P0.05);与I/R组比较,SPC组神经行为学评分降低,脑梗死面积减少(P0.05);(2)与Sham组比较,I/R组和SPC组脑组织Iba-1蛋白表达水平上调,脑组织MDA、TNF-α和IL-1β含量增加,ROS活性增强,SOD活性降低,脑组织HO-1蛋白表达水平下调(P0.05);与I/R组比较,SPC组脑组织Iba-1蛋白表达水平下调,脑组织MDA、TNF-α和IL-1β含量和ROS活性降低,SOD活性增强,脑组织HO-1蛋白表达水平上调(P0.05);结论:七氟醚后处理可能通过抑制脑缺血再灌注时诱发的小胶质细胞激活,减轻大鼠脑组织氧化应激及炎症反应,进而发挥其对大鼠脑缺血再灌注损伤的保护作用。
[Abstract]:Aim: to evaluate the effects of sevoflurane postconditioning on oxidative stress and inflammatory response during cerebral ischemia-reperfusion in rats and to explore the protective mechanism of sevoflurane. Methods: 36 male clean grade healthy SD rats, weighing 220 ~ 260 g / 12 weeks old, were randomly divided into 3 groups: sham operation group (Sham group). Cerebral ischemia-reperfusion (I / R) group and sevoflurane post-treatment group (SPC group) with 12 rats in each group. I / R group and SPC group were used to establish cerebral ischemia-reperfusion injury model. Rats in the Sham group did not block the middle cerebral artery. The SPC group received inhalation of 2.6% sevoflurane for 15 min. immediately after reperfusion. At the end of 24 h after reperfusion, the neurobehavioral score was assessed by Longa method. The rats in each group were killed and the brain tissues were taken out. The expression of Iba-1 and HO-1 protein was detected by TTC staining, and the expression of Iba-1 and HO-1 protein was detected by, Western blot method, and the ROS, of brain tissue was measured by TTC staining. The levels of SOD,MDA,TNF- 伪 and IL-1 尾. Results: (1) compared with Sham group, I / R group and SPC group increased neurobehavioral score and cerebral infarction area (P0.05), compared with I / R group, SPC group decreased neurobehavioral score and cerebral infarction area (P0.05). (2) compared with Sham group, the expression of Iba-1 protein in brain tissue of I / R group and SPC group was up-regulated, the contents of MDA,TNF- 伪 and IL-1 尾 in brain tissue were increased, the activity of ROS was increased, and the activity of SOD was decreased. The expression of HO-1 protein in brain tissue was down-regulated (P0.05). Compared with I / R group, the expression of Iba-1 protein was down-regulated, the contents of MDA,TNF- 伪 and IL-1 尾 and the activity of ROS were decreased, the activity of SOD was increased, and the expression of HO-1 protein was up-regulated in SPC group (P0.05). Conclusion: sevoflurane post-treatment may reduce oxidative stress and inflammation by inhibiting the activation of microglia induced by cerebral ischemia-reperfusion in rats and then exert its protective effect on cerebral ischemia-reperfusion injury in rats.
【学位授予单位】：南昌大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R614
本文编号：2307233
[Abstract]:Aim: to evaluate the effects of sevoflurane postconditioning on oxidative stress and inflammatory response during cerebral ischemia-reperfusion in rats and to explore the protective mechanism of sevoflurane. Methods: 36 male clean grade healthy SD rats, weighing 220 ~ 260 g / 12 weeks old, were randomly divided into 3 groups: sham operation group (Sham group). Cerebral ischemia-reperfusion (I / R) group and sevoflurane post-treatment group (SPC group) with 12 rats in each group. I / R group and SPC group were used to establish cerebral ischemia-reperfusion injury model. Rats in the Sham group did not block the middle cerebral artery. The SPC group received inhalation of 2.6% sevoflurane for 15 min. immediately after reperfusion. At the end of 24 h after reperfusion, the neurobehavioral score was assessed by Longa method. The rats in each group were killed and the brain tissues were taken out. The expression of Iba-1 and HO-1 protein was detected by TTC staining, and the expression of Iba-1 and HO-1 protein was detected by, Western blot method, and the ROS, of brain tissue was measured by TTC staining. The levels of SOD,MDA,TNF- 伪 and IL-1 尾. Results: (1) compared with Sham group, I / R group and SPC group increased neurobehavioral score and cerebral infarction area (P0.05), compared with I / R group, SPC group decreased neurobehavioral score and cerebral infarction area (P0.05). (2) compared with Sham group, the expression of Iba-1 protein in brain tissue of I / R group and SPC group was up-regulated, the contents of MDA,TNF- 伪 and IL-1 尾 in brain tissue were increased, the activity of ROS was increased, and the activity of SOD was decreased. The expression of HO-1 protein in brain tissue was down-regulated (P0.05). Compared with I / R group, the expression of Iba-1 protein was down-regulated, the contents of MDA,TNF- 伪 and IL-1 尾 and the activity of ROS were decreased, the activity of SOD was increased, and the expression of HO-1 protein was up-regulated in SPC group (P0.05). Conclusion: sevoflurane post-treatment may reduce oxidative stress and inflammation by inhibiting the activation of microglia induced by cerebral ischemia-reperfusion in rats and then exert its protective effect on cerebral ischemia-reperfusion injury in rats.
【学位授予单位】：南昌大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R614
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相关期刊论文 前3条
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