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目的:从细胞炎性因子方面揭示毒素清颗粒对克雷伯杆菌肺炎所致多器官损伤保护作用机制。方法:将55只老龄大鼠随机分为空白对照组、模型组、毒素清组和洛美沙星组,模型组25只,其余3组均为10只;采用气管插管法注入肺炎克雷伯杆菌制备肺炎致多器官损伤动物模型;观察肺、心、小肠等组织炎性因子白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)表达变化。结果:与空白对照组比较,模型组肺、心、肾、小肠组织TNF-α,IL-1,IL-6表达水平明显增高(P<0.01或P<0.05);外周血白细胞计数、中性粒细胞亦显著增高(P<0.01);脏器组织学发生了明显的病理改变(P<0.01或P<0.05)。与模型组比较,毒素清组肺、心、小肠、肾TNF-α,IL-1,IL-6蛋白表达明显降低(P<0.01或P<0.05);白细胞计数和中性粒细胞明显降低(P<0.01);脏器损伤程度明显减轻(P<0.01或P<0.05)。结论:降低组织炎性因子IL-1,IL-6,TNF-α表达水平,从而减轻脏器损伤,可能是毒素清对老年多器官损伤保护作用的主要机制之一。
OBJECTIVE: To reveal the protective mechanism of toxin granules against multiple organ injury induced by Klebsiella pneumoniae in terms of cellular inflammatory factors. Methods: Fifty-five aged rats were randomly divided into blank control group, model group, toxin group and lomefloxacin group, model group 25, and the remaining three groups were 10; tracheal intubation into Klebsiella pneumoniae Bacillus was used to prepare multiple organ injury model induced by pneumonia. The inflammatory cytokines such as IL-1, IL-6, TNF, -α) expression changes. Results: Compared with the blank control group, the expression levels of TNF-α, IL-1 and IL-6 in lung, heart, kidney and small intestine of model group were significantly increased (P <0.01 or P < Granulocytes were also significantly increased (P <0.01). Significant pathological changes were found in histology (P <0.01 or P <0.05). Compared with the model group, the expression of TNF-α, IL-1 and IL-6 in the lung, heart, small intestine and kidney of the Toxin group was significantly lower (P <0.01 or P <0.05); the WBC and neutrophils were significantly decreased P <0.01). The extent of organ damage was significantly reduced (P <0.01 or P <0.05). CONCLUSION: It is one of the main mechanisms of protection of toxins on senile multiple organ injury by reducing the expression of tissue inflammatory factors IL-1, IL-6 and TNF-α, thereby reducing organ damage.