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作 者:王松林[1] 李东波[1] 杨涛[1] 李从进[1] 宋锦宁[2] 金涛[1] WANG Songlin;LI Dongbo;YANG Tao;LI Congjin;SONG Jinning;JIN Tao(Department of Neurosurgery,Ankang City Central Hospital,Ankang 725000,China;Department of Neurosurgery,First Affiliated Hospital of Xi’an Jiaotong University)
机构地区:[1]陕西省安康市中心医院神经外科,安康725000 [2]西安交通大学第一附属医院神经外科
出 处:《山西医科大学学报》2021年第2期179-183,共5页Journal of Shanxi Medical University
基 金:教育部新世纪优秀人才支持计划资助项目(NCET-05-0831)。
摘 要:目的研究冬凌草甲素(Ori)减轻大鼠脑外伤(TBI)的作用及机制。方法36只雄性SD大鼠按随机数字表法分为对照组、TBI 3 d组和TBI 3 d+Ori组,每组12只。对照组仅接受麻醉,TBI 3 d组利用Feeney法自由落体颅脑损伤装置建立大鼠TBI模型,TBI 3 d+Ori组在造模后立刻腹腔注射冬凌草甲素(1 mg/100 g),此后每12 h给药1次,连续3 d。利用免疫组化检测GFAP、Iba-1的表达,TUNEL检测细胞凋亡,ELISA检测TNF-α、IL-1β和IL-6的水平;Western blot检测细胞核内NF-κB表达及细胞质内p38 MAPK的磷酸化。结果与对照组相比,TBI 3 d组GFAP、Iba-1、TNF-α、IL-1β、IL-6、细胞核内NF-κB的表达及p38 MAPK的磷酸化水平均升高,细胞凋亡增加(均P<0.05);与TBI 3 d组相比,TBI 3 d+Ori组GFAP、Iba-1、TNF-α、IL-1β、IL-6、细胞核内NF-κB的表达及p38 MAPK的磷酸化水平均下降,细胞凋亡数减少(均P<0.05)。结论冬凌草甲素能减少TBI后TNF-α、IL-1β和IL-6的释放,抑制胶质反应,减轻脑损伤,其作用可能与阻断NF-κB及p38 MAPK途径有关。Objective To study the protective effect and its mechanism of oridonin(Ori)against traumatic brain injury(TBI)in rats.Methods Thirty-six SD male rats were equally divided into control group,TBI 3 d group and TBI 3 d+Ori group according to the random number table method.Rats in control group were only anesthetized.TBI models were established by Feeney DM device.Rats in TBI 3 d+Ori group were intraperitoneally injected with Ori after injury immediately(1 mg/100 g),twice a day for consecutive 3 d.The expression of GFAP and Iba-1 was detected by immunohistochemistry.Cell apoptosis was detected by TUNEL.The levels of TNF-α,IL-1β and IL-6 were assessed by ELISA.The expression of NF-κB in cell nucleus and the phosphorylation of p38 MAPK were accessed by Western blot.Results Compared to control group,the expression of GFAP,Iba-1,TNF-α,IL-1β,IL-6,NF-κB,phosphorylation of p38 MAPK and the number of cell apoptosis were significantly increased in TBI 3 d group(P<0.05).Compared to TBI 3 d group,the expression of GFAP,Iba-1,TNF-α,IL-1β,IL-6,NF-κB,phosphorylation of p38 MAPK and the number of cell apoptosis were significantly decreased in TBI 3 d+Ori group(P<0.05).Conclusion Oridonin can alleviate the brain injury,reduce the release of TNF-α,IL-1β,IL-6 and inhibit the glial response and cell apoptosis.The protective mechanism of Ori might be related to NF-κB and p38 MAPK pathway.
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