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[目的]探讨醒脑静注射液对兔内毒素休克时肾功能的保护作用及可能机制。[方法]日本大耳白兔18只,随机分为正常对照组、LPS组、LPS+XNJ组,每组各6只。用耳沿静脉推注LPS复制兔内毒素休克模型。于0h、1h、2h、3h取血测定尿素氮(BUN),血清肌酐(Scr),检测血浆TNF-α的含量。半定量RT-PCR检测肾脏TLR-4基因的表达。[结果](1)血清BUN的变化:LPS组血清BUN持续明显升高,LPS+XNJ组BUN升高不明显。(2)血清Scr的变化:LPS组血清Scr明显升高,LPS+XNJ组Scr0h升高,2h达到最高,3h下降。(3)TNF-α的变化:LPS组TNF-α0h开始增高,3h达到顶峰;LPS+XNJ组TNF-α在0h达到顶峰,1h明显下降,3h降至最低。(4)IL-10的变化:LPS组IL-10在3h达到顶峰,PLS+XNJ组在2h达到顶峰,3h开始下降。(5)肾脏组织TLR4mRNA的表达:LPS组术后3h肾脏TLR4mRNA表达量明显增加,LPS+XNJ组肾脏TLR4mRNA表达量较LPS组明显减少。[结论]醒脑静注射液对内毒素休克时家兔肾功能有保护作用,其作用机制可能是通过抑制TLR4的表达,抑制NF-KB的活化,从而抑制炎性因子TNF-a释放来实现的。
[Objective] To explore the protective effect of Xingnaojing injection on renal function in rabbits with endotoxin shock and its possible mechanism. [Method] Eighteen Japanese white rabbits were randomly divided into normal control group, LPS group, LPS + XNJ group, 6 rats in each group. Rabbit endotoxin shock model was replicated by injecting LPS along the vein. The levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were measured at 0h, 1h, 2h and 3h after injection. The levels of plasma TNF-α were measured. Semi-quantitative RT-PCR detection of renal TLR-4 gene expression. [Results] (1) The changes of serum BUN: The serum BUN in LPS group continued to increase significantly, while the BUN in LPS + XNJ group was not obvious. (2) Changes of serum Scr: Scr of LPS group was significantly increased, Scr0h increased in LPS + XNJ group, reached the highest at 2h and decreased at 3h. (3) The changes of TNF-α: TNF-α0h began to increase in LPS group and peaked at 3h; TNF-α peaked at 0h in LPS + XNJ group, decreased significantly at 1h, and reached the lowest at 3h. (4) Changes of IL-10: IL-10 peaked at 3h in LPS group, peaked at 2h in PLS + XNJ group, and decreased at 3h. (5) The expression of TLR4mRNA in kidney: The expression of TLR4mRNA in kidney increased significantly 3h after operation in LPS group, while the expression of TLR4mRNA in LPS + XNJ group was significantly lower than that in LPS group. [Conclusion] Xingnaojing injection has a protective effect on renal function in rabbits with endotoxin shock, and its mechanism may be through inhibiting the expression of TLR4, inhibiting the activation of NF-KB and inhibiting the release of inflammatory factor TNF-a of.