宋雅妹1 张薇1△ 梁蕊2 巩翠珂1 周慧会1.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[J].,2012,12(24):4633-4637 |
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 |
The Analysis of Leptin and Interleukin-8 Expression in Rat Models ofChronic Obstructive Pulmonary Disease |
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DOI: |
中文关键词: 慢性阻塞性肺疾病 瘦素 白介素-8 内毒素 |
英文关键词: Chronic obstructive pulmonary disease Leptin Interleukin-8 LPS |
基金项目: |
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中文摘要: |
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。 |
英文摘要: |
Objective: To investigate the expression matter of leptin and IL-8 in rat models of COPD, and analyse their relevance,
investigate the value of leptin in the development of COPD. Methods: 36 Male SD rats were randomly divided into 3 groups: (1) Control
group: untreated rats;(2)COPD1: rats were intratracheally administered LPS (200 μg) on d 1 and 14 and exposed to 5% smoke for 2 h
daily for 4 consecutive weeks;(3)COPD2: rats were exposed to 5% smoke for 2 h daily for 12 consecutive weeks. To observe the
pathological changes of the lung tissues, and take immunohistochemistry to determine leptin and IL-8 levels expressed in bronchial lung
tissue. Serum leptin and IL-8 concentration was examined by radio-immunity method. Results: The cell factor leptin and inflammatory
factor IL-8 in bronchial lung tissue were positive expressed. The expression of leptin ( 52.67±04.72)and IL-8 (59.56±3.94) in COPD 1
group was higher than that in COPD2 group leptin(38.89±2.57)and IL-8(55.22±3.42), P<0.05; Both leptin and IL-8 expression in two
COPD model groups were higher than that in the normal group (16.90±1.52) and (28.00±4.24), P<0.05; In the COPD1 group, serum
leptin level (3.26±0.95) ng/mL and IL-8(107.51±13.38) levels were markedly higher than that in the COPD2 group(2.42±0.69)ng/ml
and (94.07±11.20) pg/mL, P < 0.05, and these levels in both COPD groups increased dramatically compared with that in controls
(0.95±0.56)ng/mL and IL-8 (39.48±6.35) pg/mL, P<0.05. There was negative correlation between leptin and IL-8 expression(r=0.72
0.67 0.84 all P<0.05)in blood. The comparison between the two groups had statistical significance after inspection. Conclusion: Leptin
and IL-8 play important roles in the occurrence and development of COPD, which is correlated with each other. In addition, LPS
facilitates the expression of leptin and IL-8. |
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