摘要
目的初步探讨Toll样受体4(TLR4)在脑梗死炎性损伤中的作用,观察TLR4 mRNA表达及与TNF-α浓度的动态相关性,旨在探索急性脑梗死缺血炎性损伤的病生机制,为临床治疗脑梗死提供新的治疗靶点。方法分别运用RT-PCR法、ELISA法测定脑梗死发病第1天、第2天、第7天外周血单个核细胞(淋巴细胞、单核细胞)TLR4 mRNA表达及血清TNF-α浓度。结果 TLR4 mRNA、血清TNF-α在脑梗死的急性期均呈上升趋势,而TLR4 mRNA的表达在发病的第1天即明显升高,第3天达到较高水平,第7天持续在高水平的平台期。血清TNF-α浓度在第1天略升高,第3天呈大幅度上升,第7天达最高值。脑梗死(第3天)外周血单个核细胞TLR4 mRNA表达与血清浓度TNF-α呈正相关。脑梗死体积越大,TLR4 mRNA表达越高。结论脑梗死患者急性期TLR4 mRNA表达增加有可能是TNF-α产生、分泌增多的上游启动环节,从而参与介导脑缺血炎性损伤。
Objective To study the role of Toll-like receptor 4 in the inflammatory injury of acute cerebral infarction and the dynamic correlation between TNF-α concentration and TLR4mRNA expression,in order to further explore the pathological mechanism of cerebral ischemic injury and provide new way for the management of acute cerebral infarction.Methods RT-PCR and ELISA were respectively used to measure expression of the TLR4 mRNA in the peripheral lymphocytes and monocytes,TNF-α concentration in the serum at the 1st day,the 3rd day and the 7th day after onset.Results TLR4 mRNA expression and the TNF-α concentration at the acute stage both displayed the evident increasing tendency. The TLR4 mRNA expression increased at the 1st day,continued to greatly increase at the 3rd day,and kept the same high level at the 7th day,which shaped a platform between the 3rd day and the 7th day. TNF-α concentration in serum at the 1st day was only slightly elevated ,drastically increased at the 3rd day,and reached the peak of the sever days after onset at the 7th day. TLR4 mRNA expression correlated positively with TNF-α concentration at the 3rd day after acute cerebral infarction onset. The larger infarct volume was,the higher TLR4 mRNA expression was.Conclusion The expression of the TLR4 mRNA in the peripheral lymphocyte and monocyte during acute cerebral infarction are elevated,which may play a critical role in the cerebral isocheimal inflammatory injury mechanism through spurring the production and excretion of inflammatory factor TNF-α.
出处
《海南医学》
CAS
2010年第17期1-5,共5页
Hainan Medical Journal
关键词
脑梗死
TOLL样受体4
肿瘤坏死因子-Α
炎性损伤
Acute cerebral infarction
Toll-like receptor4
Tumor necrosis factor-α
Inflammatory injury
