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炎性因子在脑缺血——再灌注不同时期的基因表达 被引量:6

The gene expression of pro-inflammatory cytokines at different durations of cerebral ischemia reperfusion
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摘要 目的 探讨白介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)和细胞间黏附分子1(ICAM-1)在脑缺血一再灌注不同时期的基因表达。方法 将Wistar大鼠随机分为假手术组和脑缺血30 min再灌注6 h(IR6h)、12h(IR12h)、24 h(IR24h)、48 h(IR48h)组。动物模型采用线栓法制备大鼠中动脉栓塞法,用RT-PCR法检测脑缺血一再灌注不同时间点IL-1β、TNF-α及ICAM-1的表达。结果 IL-1β、TNF-α及ICAM-1在假手术组脑组织内低水平表达。IL-1βmRNA的表达在脑缺血—再灌注6 h后即明显增高,12 b后表达开始减弱,24~48 h呈低水平增高。TNF-α在脑缺血—再灌注6 h表达开始上升,24 h达到高峰,48 h后开始下降。ICAM-1脑缺血—再灌注6 h表达开始升高,24 h达到高峰,48 h后仍维持较高水平。结论 炎症因子参与了脑缺血—再灌注性损伤,且具有明显的时间规律。 Objective To explore the gene expression of pro-inflammatory cytokines after different durations of cerebral ischemia reperfusion. Methods Rats were randomly divided into five groups:sham group, 30min of cerebral ischemia after 6h, 12h, 24h and 48h groups. Transient focal ischemia/reperfusion model in male Wistar rats were induced by middle cerebral artery occlusion(MCAO) according to the intraluminal filament technique as described. The expression of pro-inflammatory cytokines including interleukin-1β(IL-1β), tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) were measured using RT-PCR. Results The gene expression of IL-1β, TNF-α, ICAM-1 was low in sham group. The mRNA expression of IL-1β was significantly increased and reached the peak after 6h,but began a decrease after 12h and kept the low level at 24h and 48h. The mRNA expression of TNF-α gradually increased after 6 h,and reached the highest levels at 24h, then began to decrease at 48h. The mRNA expression of ICAM-1 gradually increased following cerebral ischemia, and reached the peak at 24h and 48h. Conclusion Our results demonstrated that cerebral ischemia reperfusion could induce the up- regulation of IL-1β,TNF-α and ICAM-1 in a time-dependent way.
出处 《济宁医学院学报》 2014年第4期240-243,共4页 Journal of Jining Medical University
基金 山东省自然科学基金项目(编号:2012GSF11806) 国家自然科学基金项目(编号:81070961)
关键词 脑缺血 炎症反应 神经损伤 Cerebral ischemia Inflammation Neural damage
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  • 1Gu L,Huang B,Shen W,et al. Early activation of nSMase2/ceramide pathway in astrocytes is involved in ischemia-associ-ated neuronal damage via inflammation in rat hippocampi[J].J Neuroinflammation,2013,10(1) : 109.
  • 2Guan 丁,Liu Q,Qian Y, et al. Ruscogenin reduces cerebral is-chemic injury via NF-tcB-mediated inflammatory pathway inthe mouse model of experimental stroke [J]. European JPharmacol,2013,714(1) :303-311.
  • 3Longa EZ, Weinstein PR, Carlson S, et al. Reversible middlecerebral artery occlusion without craniectomy in rats C J3-Stroke,1989,20(1):84-91.
  • 4李金国,白波.线栓法制备大鼠局灶性脑缺血模型的研究[J].泰山医学院学报,2008,29(4):308-312. 被引量:6
  • 5蔡世昌,张秋玲,李金国,白波.Apelin对急性局灶性脑缺血再灌注损伤大鼠脑神经细胞的保护作用[J].第二军医大学学报,2012,33(12):1324-1328. 被引量:6
  • 6Vasiljevic B, Maglajlic - Djukic S, Gojnic M, et al. New in-sights into the pathogenesis of perinatal hypoxic - ischemicbrain injury[J]. Pediatr Int,2011,53(4) :454-462.
  • 7Wang X, Zhang J, Si D, et al. Progesterone inhibits the ex-pression of cycloxygenase-2 and interleukin-1 [3 in neonatalrats with hypoxic ischemic brain damage[J]. Int J Neurosci,2014,124(1):42-48.
  • 8Zhang S,Qi Y,Xu Y,et al. Protective effect of flavonoid-richextract from Rosa laevigata Michx on cerebral ischemia-reperfusion injury through suppression of apoptosis and in-flammation[J]. Neurochem Int,2013 ,63(5) : 522-532.
  • 9He W,Chen W,Zhou Y,et al. Xanthotoxol exerts neuropro-tective effects via suppression of the inflammatory responsein a rat model of focal cerebral ischemia[J], Cell Mol Neuro-bioi,2013,33(5):715-722.
  • 10Maddahi A,Edvinsson L. Cerebral ischemia induces microvas-cular pro-inflammatory cytokine expression via the MEK/ERK pathway[J]. J Neuroinflammation,2010,7(1) : 14.

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