【摘要】：目的:評(píng)價(jià)七氟醚后處理對(duì)大鼠腦缺血再灌注時(shí)氧化應(yīng)激及炎癥反應(yīng)的影響,以探討其腦保護(hù)的作用機(jī)制。方法:雄性清潔級(jí)健康SD大鼠36只,體重220~260 g,12~14周齡,采用隨機(jī)數(shù)字表法分為3組:假手術(shù)組(Sham組)、腦缺血再灌注組(I/R組)和腦缺血再灌注+七氟醚后處理組(SPC組),每組12只。I/R組和SPC組采用線栓法建立腦缺血再灌注損傷模型,缺血30 min,再灌注24 h;Sham組大鼠不阻塞大腦中動(dòng)脈。SPC組于再灌注即刻給予吸入2.6%的七氟醚15 min。于再灌注24 h末采用Longa法進(jìn)行神經(jīng)行為學(xué)評(píng)分,處死各組大鼠,取腦組織,采用TTC法染色測(cè)定腦組織的梗死面積、Western blot法檢測(cè)Iba-1和HO-1蛋白表達(dá)水平,測(cè)定腦組織ROS、SOD、MDA、TNF-α和IL-1β的水平。結(jié)果:(1)與Sham組比較,I/R組和SPC組神經(jīng)行為學(xué)評(píng)分升高,腦梗死面積增加(P0.05);與I/R組比較,SPC組神經(jīng)行為學(xué)評(píng)分降低,腦梗死面積減少(P0.05);(2)與Sham組比較,I/R組和SPC組腦組織Iba-1蛋白表達(dá)水平上調(diào),腦組織MDA、TNF-α和IL-1β含量增加,ROS活性增強(qiáng),SOD活性降低,腦組織HO-1蛋白表達(dá)水平下調(diào)(P0.05);與I/R組比較,SPC組腦組織Iba-1蛋白表達(dá)水平下調(diào),腦組織MDA、TNF-α和IL-1β含量和ROS活性降低,SOD活性增強(qiáng),腦組織HO-1蛋白表達(dá)水平上調(diào)(P0.05);結(jié)論:七氟醚后處理可能通過(guò)抑制腦缺血再灌注時(shí)誘發(fā)的小膠質(zhì)細(xì)胞激活,減輕大鼠腦組織氧化應(yīng)激及炎癥反應(yīng),進(jìn)而發(fā)揮其對(duì)大鼠腦缺血再灌注損傷的保護(hù)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- 偽 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- 偽 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- 偽 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.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R614

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本文編號(hào)：2307233