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促炎细胞因子在细菌性肺炎老龄大鼠多器官损伤中的作用 被引量:2

Roles of proinflammatory factors in infectious multiple organ injury in aged rats
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摘要 目的探讨促炎细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、IL-6在老年感染性多器官损伤中的意义。方法将大鼠随机分为青年对照组、青年模型组和老龄对照组、老龄模型组;采用气管插管法注入肺炎克雷们杆菌,由肺炎导致多器官损伤;应用光学显微镜、免疫组织化学技术,观察肺、心、小肠及肾脏组织病理改变与促炎细胞因子TNF-α、IL-1、IL-6变化情况。结果与同龄对照组比较,老龄模型组和青年模型组肺、心、肾、小肠组织TNF-α、IL-1、IL-6表达水平明显增高及脏器组织病理学改变明显(P<0.01或P<0.05);而老龄模型组肺IL-1、心TNF-α、IL-6和小肠IL-1、IL-6表达水平又较青年模型组显著增高(P<0.01或P<0.05),脏器损伤亦较重(P<0.05)。结论促炎细胞因子TNF-α、IL-1、IL-6参与了老年感染性多器官损伤,并在其中发挥了重要作用。 Objective To investigate the roles of proinflammatory factors,including tumor necrosis factor-alpha(TNF-α), interleukin-1(IL-1) and IL-6 in the infectious multiple organ injury in aged rats.Methods Male SD rats were randomly divided into young control group(YCG,n=10),young model group(YMG,n=15),elderly control group(ACG,n=10) and elderly model group(AMG, n=25).Multiple organ injury was induced by injection of Klebsiella pneumoniae through tracheal intubation in rat models of pneumonia. The pathological changes of lungs,heart,kidneys,and small intestine were investigated immunohistochemically.The changes of proinflammatory factors expression in these tissues were also observed.Results The expression levels of TNF-α,IL-1,and IL-6 in lungs,heart,kidneys and small intestine were significantly higher in YMG and AMG than in YCG and ACG(P0.01 or P0.05).The pathological changes of lungs,heart,kidney and small intestine were more obvious in YMG and AMG than in YCG and ACG(P0.01 or P0.05).The expression levels of IL-1 in lungs,TNF-αand IL-6 in heart,and IL-1 and IL-6 in small intestine were significantly elevated,and organ injuries were severer in ACG than in YCG(P0.01 or P0.05).Conclusion Proinflammatory factors,including TNF-α,IL-1 and IL-6,play important roles in the development of infectious multiple organ injury in the aged rats.
出处 《中华老年多器官疾病杂志》 2011年第5期439-442,共4页 Chinese Journal of Multiple Organ Diseases in the Elderly
基金 河南省高校新世纪优秀人才支持计划(NO 2006HANCET-05)~~
关键词 感染 大鼠 多器官功能衰竭 肿瘤坏死因子-α 白细胞介素类 inflammation rat multiple organ failure tumor necrosis factor interleukin
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