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目的观察脑出血后大鼠继发内毒素血症的炎症效应,并探讨利开灵对其影响。方法采用Rosenberg法改良后建立大鼠脑出血模型,根据脑出血不同时点(12、24、48、72小时)分为4组,每个时间点再分为3组:假手术组、模型组、利开灵组,用终点显色法检测各组血浆内毒素(LPS)水平,ELISA法检测各组血清肿瘤坏死因子α(TNF-α)、白介素1β(IL-1β)水平,放射免疫法检测各组出血局部脑组织TNF-α、IL-1β水平。结果模型组LPS均明显升高,在48小时达高峰(P<0.01);血清TNF-α、IL-1β升高,均在24小时达高峰(P<0.01);出血局部脑组织TNF-α升高,呈上升趋势直至72小时,IL-1β呈先升高再下降的趋势,在48小时达最高(P<0.01)。同时发现利开灵可下调血浆LPS、血清和出血局部脑组织TNF-α、IL-1β过高表达。结论脑出血后大鼠继发内毒素血症,并且引发体内炎症反应和加重脑局部的炎症反应。利开灵对脑出血继发内毒素血症的炎症效应有较好的调控作用,这可能是利开灵改善脑出血后脑水肿的作用机制之一。
Objective To observe the inflammatory effects secondary to endotoxemia in rats after intracerebral hemorrhage and to investigate the effect of LiKailing on it. Methods The rat model of intracerebral hemorrhage was established by Rosenberg method and divided into 4 groups at different time points (12, 24, 48 and 72 hours). The rats were divided into 3 groups at each time point: sham operation group, model group , And Likailing group. Plasma endotoxin (LPS) levels in each group were measured by end-point colorimetric method. Serum levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) were measured by ELISA. Radioimmunoassay The levels of TNF-α and IL-1β in the local brain tissue of hemorrhage in each group were detected. Results The levels of LPS in model group were significantly higher than those in control group (P <0.01), and the levels of TNF-α and IL-1β in serum increased at 24 hours (P <0.01) IL-1β increased first and then decreased at 72 hours, reaching the highest at 48 hours (P <0.01). At the same time, it was found that LiKailing down-regulated the expression of TNF-α and IL-1β in the plasma LPS, serum and hemorrhagic local brain tissue. Conclusions After intracerebral hemorrhage, secondary to endotoxemia occurs in rats and triggers inflammation in the body and aggravates inflammation in the brain. Li Kai Ling on cerebral hemorrhage secondary to endotoxemia secondary to inflammatory effects have a better regulatory effect, which may be Kai-Ling one of the mechanisms of cerebral edema after cerebral hemorrhage.