本文關鍵詞：小窩蛋白-1在呼吸機致大鼠肺損傷發(fā)生中的作用研究　出處：《山西醫(yī)科大學》2014年碩士論文　論文類型：學位論文

  更多相關文章： 機械通氣所致肺損傷 小窩蛋白-1 P38絲裂原活化蛋白激酶 白細胞介素-8

【摘要】：目的通過觀察不同時間段肺組織中小窩蛋白-1(caveolin-1, cav-1)、p-P38MAPK和IL-8的表達水平,探討cav-1在機械通氣所致肺損傷(VILI)發(fā)生中的作用。方法雄性Wistar大鼠24只,隨機分為3組：對照組、大潮氣量通氣半小時組(H-VT0.5h組)和大潮氣量通氣2小時組(H-VT2h組)。在光鏡下觀察各組大鼠肺組織病理學改變,測定BALF總蛋白含量和肺濕/干重比值(W/D),采用免疫組織化學染色法測定肺組織cav-1、p-P38MAPK和IL-8的蛋白表達水平,并進行相關性分析。 結果 1.肺組織cav-1表達結果：H-VT0.5h組(0.142±0.014)和H-VT2h組(0.267+0.017)cav-1蛋白表達均明顯高于對照組(0.118±0.010)(均P0.01),H-VT2h組cav-1蛋白表達明顯高于H-VT0.5h組(P0.01)。 2.肺組織IL-8表達結果：H-VT2h組(0.609±0.095)IL-8蛋白表達明顯高于對照組(0.145+0.057)和H-VT0.5h組(0.190±0.048)(均P0.01),對照組和H-VT0.5h組比較差異無統(tǒng)計學意義(P0.05)。 3.肺組織P-P38MAPK表達結果：H-VT2h組(0.514±0.031)p-P38MAPK蛋白表達明顯高于對照組(0.148±0.016)和H-VT0.5h組(0.166+0.010)(均P0.01),對照組和H-VT0.5h組比較差異無統(tǒng)計學意義(P0.05)。 4.肺組織cav-1、p-P38MAPK、IL-8相關性分析結果：各組大鼠肺組織中cav-1蛋白表達與p-P38MAPK之間呈正相關(r=0.787,P0.01)；肺組織cav-1表達水平與IL-8之間也呈正相關(r=0.737,P0.01)。 5.肺組織W/D比值測定結果：H-VT2h組(6.460±0.740)W/D比值明顯高于對照組(4.200±0.320)和H-VT0.5h組(4.440±0.510)(均P0.01),H-VT0.5h組與對照組比較差異無統(tǒng)計學意義(P0.05)。 6.BALF總蛋白含量測定結果：H-VT2h組(0.620±0.140)BALF中總蛋白含量明顯高于對照組(0.220±0.063)和H-VT0.5h組(0.300±0.140)(均P0.01),H-VT0.5h組與對照組比較差異無統(tǒng)計學意義(P0.05)。 7.肺組織病理學結果：隨著機械通氣時間延長,大鼠肺組織損傷程度呈逐漸加重趨勢。結論 1.大潮氣量機械通氣誘導了cav-1的表達,早期(0.5h內(nèi))以保護作用為主,后期(2h后)以損傷作用為主。 2.cav-1通過激活P38MAPK信號通路,使IL-8等炎癥因子表達增多,可能是導致VILI發(fā)生的重要途徑之一。
[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 鹵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 鹵0. 095) and 0. 145 0. 057 in the control group (n = 0. 609 鹵0. 095). And H-VT 0.5h group 0.190 鹵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 鹵0. 031). 0.148 鹵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 鹵0.740 W / D vs 4.200 鹵0.320). And H-VT 0.5h group (4.440 鹵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 鹵0. 063). And H-VT 0.5h group (0.300 鹵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.
【學位授予單位】：山西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R563.8

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