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作 者:张国栋[1] 孙来广[1] 张家旗 李远超 程振国[1] Zhang Guodong;Sun Laiguang;Zhang Jiaqi;Li Yuanchao;Cheng Zhenguo(Department of Neurosurgery,Xinxiang Central Hospital,Xinxiang 453000,Henan Province,China)
出 处:《中华麻醉学杂志》2019年第9期1143-1146,共4页Chinese Journal of Anesthesiology
摘 要:目的评价七氟醚麻醉对大鼠创伤性颅脑损伤(TBI)时小胶质细胞极化的影响。方法健康成年雄性SD大鼠72只,体重230~250 g,采用随机数字表法分为3组(n=24):假手术组(Sham组)、TBI组和TBI+七氟醚麻醉组(TBI+Sevo组)。TBI组和TBI+Sevo组采用Feeney法制备大鼠TBI模型,30 min后TBI+Sevo组吸入2.4%七氟醚1 h,1次/d,连续3 d,Sham组和TBI组吸入纯氧。分别于造模后1、3、7和14 d时,随机取6只大鼠,行改良神经功能评分(mNSS);取尾静脉血标本,采用ELISA检测血清TNF-α、IL-1β和IL-6浓度;然后处死大鼠取脑挫裂伤灶边缘皮质组织,采用TUNEL法测定细胞凋亡情况,计算细胞凋亡率,分别采用免疫荧光法和Western blot法检测小胶质细胞标志物Iba-1、M1型小胶质细胞标志物CD86和M2型小胶质细胞标志物CD206表达。结果与Sham组比较,TBI组和TBI+Sevo组mNSS、皮质组织细胞凋亡率、Iba-1、CD86和CD206表达水平、血清TNF-α、IL-1β和IL-6浓度升高(P<0.05);与TBI组比较,TBI+Sevo组mNSS、皮质组织细胞凋亡率、Iba-1和CD86表达水平、血清TNF-α、IL-1β和IL-6浓度降低,CD206表达上调(P<0.05)。结论七氟醚麻醉减轻大鼠TBI的机制可能与促进小胶质细胞极化,抑制全身炎症反应有关。Objective To evaluate the effects of sevoflurane on microglial polarization after traumatic brain injury(TBI)in rats.Methods Seventy-two healthy adult male Sprague-Dawley rats,weighing 230-250 g,were divided into 3 groups(n=24 each)using a random number table method:sham operation group(group Sham),group TBI,and TBI plus sevoflurane anesthesia group(group TBI+Sevo).TBI models were established by using Feeney′s method in TBI and TBI+Sevo groups,30 min later 2.4%sevoflurane was inhaled for 1 h once a day for 3 consecutive days in TBI+Sevo group,while pure oxygen was inhaled instead in Sham and TBI groups.At 1,3,7 and 14 days after establishing the model,6 rats were selected,the neurological function was evaluated with the modified neurologic severity score(mNSS),and tail venous blood samples were taken for determination of tumor necrosis factor-a(TNF-α),interleukin-1beta(IL-1β)and IL-6 concentrations by enzyme-linked immunosorbent assay.The rats were then sacrificed,the limbic cortical tissues of brain contusion lesion were taken for determination of cell apoptosis(by TUNEL)and expression of microglial marker Iba-1,microglial M1 phenotypic marker CD86 and microglial M2 phenotypic marker CD206(by Western blot).Results Compared with group Sham,the mNSS score,apoptosis rate of cortical cells,expression of Iba-1,CD86 and CD206,and concentrations of serum TNF-α,IL-1βand IL-6 were significantly increased in TBI and TBI+Sevo groups(P<0.05).Compared with TBI group,the mNSS score,apoptosis rate of cortical cells,expression of Iba-1 and CD86 and concentrations of serum TNF-α,IL-1βand IL-6 were significantly decreased,and the expression of CD206 was up-regulated in TBI+Sevo group(P<0.05).Conclusion The mechanism by which sevoflurane anesthesia reduces TBI may be related to promoting microglial polarization and inhibiting systemic inflammatory response in rats.
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