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芝麻素对Toll样受体2在实验性颅脑损伤中表达的影响 被引量:4

Effect of sesamin on expression of Toll-like receptor 2 in experimental brain injury
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摘要 目的:探讨芝麻素对Toll样受体2(TLR2)在实验性颅脑损伤中表达的影响。方法:采用自由落体法建立鼠颅脑损伤模型,将45只小鼠随机分为假手术组、颅脑损伤组、脑外伤后芝麻素治疗组。称量脑组织干湿重观察脑水肿的变化;用Western blotting方法检测各组小鼠脑组织中TLR2表达;采用实时荧光定量PCR检测脑损伤周围组织中炎症因子的表达水平。结果:脑外伤组小鼠损伤侧脑水含量、TLR2表达及炎症因子表达水平较假手术组显著升高(P<0.05~P<0.01);而芝麻素治疗组的损伤侧脑水含量、TLR2蛋白表达及炎性因子表达水平则低于脑外伤组(P<0.05~P<0.01)。结论:TBI后脑组织中TLR2表达增高及炎症反应增强,而芝麻素能够抑制炎症反应,进而起到保护脑组织进一步损伤。 Objective:To investigate the effect of sesamin on the expression of Toll-like receptor 2(TLR2)in experimental brain injury.Methods:A model of craniocerebral injury was established using free fall method,and 45 mice were randomly divided into the sham surgery group,craniocerebral injury group and sesamin treatment group after brain trauma.The change of brain edema was observed by measuring the dry and wet weight of brain tissue.The expression level of TLR2 protein in brain tissue of mice was detected using Western blotting.The expression levels of inflammatory factors in tissues surrounding brain injury were detected using real time fluorescence quantitative PCR.Results:The levels of brain water,TLR2 expression and inflammatory factor in craniocerebral injury group were significantly higher than those in sham surgery group(P<0.05 to P<0.01).The levels of brain water,TLR2 protein expression and inflammatory factor expression in sesame treatment group were lower than those in craniocerebral injury group(P<0.05 to P<0.01).Conclusions:The TLR2 expression and inflammatory response in traumatic brain injury brain tissue strengthen,and sesamin can inhibit inflammatory response and protect brain tissue from further injury.
作者 吴少帅 徐福林 苏作鹏 杜嘉瑞 沈刚 WU Shao-shuai;XU Fu-lin;SU Zuo-peng;DU Jia-rui;SHEN Gang(Department of Neurosurgery,Shanghai Minhang District Central Hospital,Shanghai 201199,China)
出处 《蚌埠医学院学报》 CAS 2020年第1期23-25,共3页 Journal of Bengbu Medical College
关键词 创伤性脑损伤 TOLL样受体2 信号通路 炎症反应 芝麻素 traumatic brain injury Toll-like receptor 2 signaling pathway inflammatory response sesamin
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