小窝蛋白-1在呼吸机致大鼠肺损伤发生中的作用研究

发布时间：2018-01-02 22:01

本文关键词：小窝蛋白-1在呼吸机致大鼠肺损伤发生中的作用研究　出处：《山西医科大学》2014年硕士论文　论文类型：学位论文

【摘要】：目的通过观察不同时间段肺组织中小窝蛋白-1(caveolin-1, cav-1)、p-P38MAPK和IL-8的表达水平,探讨cav-1在机械通气所致肺损伤(VILI)发生中的作用。方法雄性Wistar大鼠24只,随机分为3组：对照组、大潮气量通气半小时组(H-VT0.5h组)和大潮气量通气2小时组(H-VT2h组)。在光镜下观察各组大鼠肺组织病理学改变,测定BALF总蛋白含量和肺湿/干重比值(W/D),采用免疫组织化学染色法测定肺组织cav-1、p-P38MAPK和IL-8的蛋白表达水平,并进行相关性分析。结果 1.肺组织cav-1表达结果：H-VT0.5h组(0.142±0.014)和H-VT2h组(0.267+0.017)cav-1蛋白表达均明显高于对照组(0.118±0.010)(均P0.01),H-VT2h组cav-1蛋白表达明显高于H-VT0.5h组(P0.01)。 2.肺组织IL-8表达结果：H-VT2h组(0.609±0.095)IL-8蛋白表达明显高于对照组(0.145+0.057)和H-VT0.5h组(0.190±0.048)(均P0.01),对照组和H-VT0.5h组比较差异无统计学意义(P0.05)。 3.肺组织P-P38MAPK表达结果：H-VT2h组(0.514±0.031)p-P38MAPK蛋白表达明显高于对照组(0.148±0.016)和H-VT0.5h组(0.166+0.010)(均P0.01),对照组和H-VT0.5h组比较差异无统计学意义(P0.05)。 4.肺组织cav-1、p-P38MAPK、IL-8相关性分析结果：各组大鼠肺组织中cav-1蛋白表达与p-P38MAPK之间呈正相关(r=0.787,P0.01)；肺组织cav-1表达水平与IL-8之间也呈正相关(r=0.737,P0.01)。 5.肺组织W/D比值测定结果：H-VT2h组(6.460±0.740)W/D比值明显高于对照组(4.200±0.320)和H-VT0.5h组(4.440±0.510)(均P0.01),H-VT0.5h组与对照组比较差异无统计学意义(P0.05)。 6.BALF总蛋白含量测定结果：H-VT2h组(0.620±0.140)BALF中总蛋白含量明显高于对照组(0.220±0.063)和H-VT0.5h组(0.300±0.140)(均P0.01),H-VT0.5h组与对照组比较差异无统计学意义(P0.05)。 7.肺组织病理学结果：随着机械通气时间延长,大鼠肺组织损伤程度呈逐渐加重趋势。结论 1.大潮气量机械通气诱导了cav-1的表达,早期(0.5h内)以保护作用为主,后期(2h后)以损伤作用为主。 2.cav-1通过激活P38MAPK信号通路,使IL-8等炎症因子表达增多,可能是导致VILI发生的重要途径之一。
[Abstract]:Objective to observe the expression levels of fossa protein 1 caveolin-1, cav-1 p38 MAPK and IL-8 in lung tissues at different time points. To investigate the role of cav-1 in the pathogenesis of lung injury induced by mechanical ventilation, 24 male Wistar rats were randomly divided into three groups: control group. The lung histopathological changes of rats in each group were observed under light microscope. The total protein content of BALF and the lung wet / dry weight ratio were measured. The expression of cav-1 p-P38 MAPK and IL-8 in lung tissue was determined by immunohistochemical staining. Correlation analysis was carried out. Results 1. The expression of cav-1 in lung tissue was 0.142 卤0.014 in 0.5 h group and 0.267 0.017 in H-VT 2 h group. The expression of cav-1 protein was significantly higher than that of control group (P 0.01). The expression of cav-1 protein in H-VT2h group was significantly higher than that in H-VT0.5h group. 2. The expression of IL-8 in lung tissue was significantly higher than that in control group (0. 609 卤0. 095) and 0. 145 0. 057 in the control group (n = 0. 609 卤0. 095). And H-VT 0.5h group 0.190 卤0.048m (all P 0.01). There was no significant difference between control group and H-VT 0.5 h group (P 0.05). 3. The expression of P-P38 MAPK in lung tissue was significantly higher than that in control group (0. 514 卤0. 031). 0.148 卤0.016) and 0.166 0.010 (all P 0.01) in H-VT 0.5h group. There was no significant difference between control group and H-VT 0.5 h group (P 0.05). 4. Cav-1p-P38MAPK in lung tissue. The results of IL-8 correlation analysis showed that there was a positive correlation between the expression of cav-1 protein and p-P38 MAPK in lung tissues of rats in each group. There was also a positive correlation between the expression of cav-1 and IL-8 in lung tissues. 5. The ratio of W / D in lung tissue was significantly higher than that in control group (6.460 卤0.740 W / D vs 4.200 卤0.320). And H-VT 0.5h group (4.440 卤0.510) (all P 0.01). There was no significant difference between H-VT 0.5 h group and control group (P 0.05). 6. The total protein content of BALF was significantly higher than that of control group (0. 220 卤0. 063). And H-VT 0.5h group (0.300 卤0.140) (all P 0.01). There was no significant difference between H-VT 0.5 h group and control group (P 0.05). 7. Results of lung histopathology: with the prolongation of mechanical ventilation time, the degree of lung injury in rats was gradually aggravated. 1. The expression of cav-1 was induced by mechanical ventilation of spring tide, which was mainly protective in the early stage and mainly in the later 2 hours. 2. Cav-1 can increase the expression of IL-8 and other inflammatory factors by activating the P38 MAPK signaling pathway, which may be one of the important pathways leading to the occurrence of VILI.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R563.8

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