慢性阻塞性肺疾病大鼠模型中痩素及白介素-8的表达分析

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目的:观察COPD大鼠模型中瘦素(leptin)、白细胞介素8(IL-8)的表达情况,分析其相关性,探讨leptin在COPD发生发展中的作用及意义。方法:36只雄性SD大鼠随机分为①健康对照组;②COPD模型1组:分别于第(1、14)d经气管内注入内毒素200ug,熏5%香烟(第1、14d除外),2h/d,共4周;③COPD模型2组:单纯熏5%香烟2h/d,共12周。观察肺组织病理变化,免疫组化法测定leptin、IL-8在支气管肺组织的表达情况,放免法测定血清leptin及IL-8浓度。结果:细胞因子leptin及炎性因子IL-8在支气管肺组织阳性表达。LPS联合熏烟诱导COPD1组支气管肺组织中leptin(52.67±04.72)和IL-8(59.56±3.94)表达较单纯熏烟诱导COPD2组leptin(38.89±2.57)和IL-8(55.22±3.42)表达明显升高,P<0.05,两组COPD大鼠模型支气管肺组织中leptin及IL-8表达较正常对照组leptin(16.90±1.52)和IL-8(28.00±4.24)表达均明显增高,P<0.05,COPD1组血清中leptin(3.26±0.95)ng/mL和IL-8(107.51±13.38)pg/mL较COPD2组中leptin(2.42±0.69)ng/mL和IL-8((94.07±11.20)pg/mL明显增高,P<0.05,两组COPD大鼠模型血清中leptin及IL-8浓度较正常对照组leptin(0.95±0.56)ng/mL和IL-8(39.48±6.35)pg/mL浓度显著升高,P<0.05。血清中Leptin与IL-8表达水平呈显著正相关(r值分别为0.72 0.67 0.84均P<0.05)。经过q检验,两两之间比较均有统计学意义。结论:leptin和IL-8均参与COPD炎症反应过程,并且具有相关性,LPS促进二者的表达。 OBJECTIVE: To observe the expression of leptin and interleukin 8 (IL-8) in COPD rat model and analyze the correlation between them and to explore the role and significance of leptin in the development of COPD. Methods: Thirty-six male Sprague-Dawley rats were randomly divided into three groups: ① healthy control group; ② COPD model group 1: Endotoxin 200ug was administered intratracheally (1,14d) 2h / d, a total of 4 weeks; ③ COPD model group 2: smoked 5% cigarettes 2h / d, a total of 12 weeks. The pathological changes of lung tissue were observed. The expressions of leptin and IL-8 in bronchial lung tissue were detected by immunohistochemistry. The levels of serum leptin and IL-8 were determined by radioimmunoassay. Results: The expression of leptin and IL-8 were positive in bronchial lung. LPS combined with fumigation induced the expression of leptin (52.67 ± 04.72) and IL-8 (59.56 ± 3.94) in bronchoalveolar lavage of COPD1 group compared with the expression of leptin (38.89 ± 2.57) and IL-8 (55.22 ± 3.42) (P <0.05). The expression of leptin and IL-8 in bronchoalveolar tissue of two groups of COPD rats were significantly higher than that of the normal control group (P <0.05), the levels of leptin (16.90 ± 1.52) and IL-8 0.05) .The leptin (3.26 ± 0.95) ng / mL and IL-8 (107.51 ± 13.38) pg / mL in COPD1 group were significantly lower than those in COPD2 group (2.42 ± 0.69 ng / mL and IL- pg / mL significantly increased (P <0.05). The concentrations of leptin and IL-8 in the two groups of COPD rats were significantly higher than those of the normal control group (0.95 ± 0.56 ng / mL and 39.88 ± 6.35 pg / mL (P <0.05) .There was a significant positive correlation between Leptin and IL-8 in serum (r = 0.72 0.67 0.84, P <0.05 respectively). Conclusion: Both leptin and IL-8 are involved in the process of COPD inflammation and are correlated with each other. LPS can promote the expression of both.
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