本文選題：重癥急性胰腺炎 + 肺損傷��； 參考：《瀘州醫(yī)學院》2014年碩士論文

【摘要】：目的：探討靜脈注射氫飽和生理鹽水對�；悄懰徕c誘導的大鼠重癥急性胰腺炎相關性肺損傷是否具有保護作用并從JNK信號通路的調(diào)控探討其作用機制。方法：1.氫飽和生理鹽水的制備：利用氫氣發(fā)生器生產(chǎn)高壓氫氣，再將高壓氫氣通入氯化鈉溶液中達到飽和濃度即可，現(xiàn)制現(xiàn)用。2.大鼠重癥急性胰腺炎相關性肺損傷模型的建立及處理：將54只健康SD雄性大鼠隨機分成假手術組（Sham組）、模型組（SAP+NS組）和氫水處理組（SAP+H2組），各組再分成6h、12h、24h三個時間點，每個時間點6只大鼠。Sham組大鼠開腹翻動胰腺數(shù)次后隨即關腹，不作其他處理，SAP+NS組和SAP+H2組以5%�；悄懰徕c（1ml/kg）經(jīng)膽胰管開口逆行注入（0.1ml/min）建立模型，在建模成功后1h經(jīng)尾靜脈分別注射等量的生理鹽水或氫飽和生理鹽水(5ml/kg)。各組分別在6h、12h、24h三個時間點處死大鼠，收集血清、肺組織及胰腺組織。用酶聯(lián)免疫吸附試驗(ELISA)法檢測血清TNF-α、IL-1β含量；分光光度計法測定肺組織中髓過氧化物酶（MPO）的活性；熒光定量PCR法檢測肺組織中TNF-α-mRNA、IL-1β-mRNA的表達；Western blot法檢測肺組織中P-JNK蛋白的表達；用肺組織濕干重比,反映肺臟水腫程度；并對胰腺組織、肺組織進行HE染色病理學檢查。以上所得數(shù)據(jù)采用均數(shù)±標準差（X—±S）表示，，運用SPSS17.0統(tǒng)計軟件進行統(tǒng)計學分析；樣本均數(shù)的比較采用方差分析；兩者的相關性采用直線相關和回歸分析，P＜0.05，則差異有統(tǒng)計學意義。結果：（1）SAP+NS組和SAP+H2組血清中TNF-α含量、肺組織中TNF-αmRNA表達水平、肺組織中P-JNK蛋白的表達、肺組織濕干重比，在6h、12h、24h各個時間點均高于Sham組（P0.05），SAP+H2組與SAP+NS組比較，SAP+H2組在各個時間點均低于SAP+H2組（TNF-α含量：204.1±8.5VS215.3±6.0，P0.05；122.4±10.3VS263.2±7.4，P0.05；84.1±8.6VS288.0±5.6，P0.05。TNF-α mRNA表達水平：2.81±0.09VS3.94±0.20，P0.05；2.51±0.11VS4.40±0.24，P0.05；1.77±0.06VS6.00±0.37，P0.05。P-JNK蛋白的表達：11.29±0.01VS11.77±0.01，P0.05；10.59±0.02VS12.73±0.01，P0.05；9.43±0.01VS14.12±0.01，P0.05。肺組織濕干重比：3.7±0.2VS4.2±0.2，P0.05；3.3±0.3VS4.9±0.2，P0.05；3.2±0.2VS4.6±0.3，P0.05。）。（2）SAP+NS組和SAP+H2組血清中IL-1β含量、胰腺和肺組織病理評分、肺組織中MPO活性、肺組織中IL-1β mRNA表達水平，在6h、12h、24h各個時間點均高于Sham組（P0.05），SAP+H2組與SAP+NS組比較，6h時無統(tǒng)計學差異，在12h、24h時SAP+H2組均低于SAP+NS組（IL-1β含量：80.3±8.3VS215.4±10.4，P0.05；59.3±8.2VS254.3±8.6，P0.05。胰腺和肺組織病理評分：7.5±1.1VS9.5±0.4，P0.05；7.3±0.4VS9.8±0.3，P0.05。4.6±0.2VS5.1±0.2，P0.05；3.8±0.3VS6.3±0.4，P0.05。MPO活性：3.3±0.2VS4.7±0.2，P0.05；3.1±0.1VS4.9±0.2，P0.05。IL-1β mRNA表達：1.77±0.16VS1.97±0.11，P0.05；1.29±0.03VS2.92±0.26，P0.05）。（3）Person相關性分析表明肺組織中P-JNK蛋白的表達與肺組織損傷程度存在相關性。結論：1.經(jīng)尾靜脈注射氫飽和生理鹽水對APALI有一定治療保護作用。2.氫飽和生理鹽水可能是通過其選擇性抗氧化作用抑制JNK細胞信號通路的激活來實現(xiàn)對APALI的保護治療作用。
[Abstract]:Objective: To explore the protective effect of intravenous hydrogen saturated saline on severe acute pancreatitis associated lung injury induced by sodium taurocholate in rats and to explore its mechanism from the regulation of JNK signaling pathway. Methods: 1. hydrogen saturated saline was prepared by hydrogen generator to produce high pressure hydrogen and then high pressure hydrogen. The establishment and treatment of the present model of severe acute pancreatitis associated lung injury in.2. rats was established and treated with saturated concentration of Sodium Chloride Solution. 54 healthy SD male rats were randomly divided into sham operation group (group Sham), model group (group SAP+NS) and hydrogen water treatment group (SAP+ H2 group), each group was then divided into 6h, 12h, 24h three time points, each time. The rats in the 6 rats of the 6 rats were operated on the pancreas to turn off the pancreas for several times and no other treatment was done. The SAP+NS group and the SAP+H2 group were injected with 5% sodium taurocholate (1ml/kg) through the biliary pancreatic duct opening retrograde injection (0.1ml/min) to establish the model. After the successful modeling, 1H was injected with equal amount of normal saline or hydrogen saturated saline (5ml/kg). The rats were killed at the three time points of 6h, 12h and 24h. The serum, lung and pancreas tissues were collected. The serum TNF- alpha and IL-1 beta content was detected by enzyme linked immunosorbent assay (ELISA); the activity of myeloperoxidase (MPO) in lung tissue was measured by spectrophotometer; the expression of TNF- alpha -mRNA, IL-1 beta -mRNA in lung tissue was detected by the fluorescence quantitative PCR method. Ern blot method was used to detect the expression of P-JNK protein in lung tissue, the ratio of wet dry weight to lung tissue was used to reflect the degree of pulmonary edema, and the pathological examination of pancreas tissue and lung tissue was carried out by HE staining. The above data were expressed with mean mean standard deviation (X - S) and SPSS17.0 statistical software was used for statistical analysis. The comparison of the average number of samples was used. The correlation was linear correlation and regression analysis. The difference was statistically significant in P < 0.05. Results: (1) the content of TNF- alpha in serum of SAP+NS and SAP+H2 group, the level of TNF- alpha mRNA in lung tissue, the expression of P-JNK protein in lung tissue, the ratio of wet dry weight in lung tissue, and higher than Sham group (P0.05) at all time points in 6h, 12h and 24h. In group AP+H2 and group SAP+NS, group SAP+H2 was lower than group SAP+H2 at all time points (TNF- alpha content: 204.1 + 8.5VS215.3 +, P0.05; 122.4 + 10.3VS263.2 + 7.4, P0.05; 84.1 + 8.6VS288.0 + 5.6, P0.05.TNF- alpha mRNA expression level: 2.81 + + 0.20, 2.51 + + 0.24, 1.77 + 0.37 The expression of NK protein: 11.29 + 0.01VS11.77 + 0.01, P0.05; 10.59 + 0.02VS12.73 + 0.01, P0.05; 9.43 + 0.01VS14.12 + 0.01, P0.05. lung tissue wet dry weight ratio: 3.7 + 0.2VS4.2 + 0.2, P0.05; 3.3 + 0.3VS4.9 + 0.2, P0.05; 3.2 + 0.2VS4.6 + 0.3. The activity of MPO in lung tissue and the expression level of IL-1 beta mRNA in lung tissue were higher than those in group Sham (P0.05) at all time points in 6h, 12h and 24h. There was no statistical difference between SAP+H2 group and SAP+NS group. Score: 7.5 + 1.1VS9.5 + 0.4, P0.05; 7.3 + 0.4VS9.8 + 0.3, P0.05.4.6 + 0.2VS5.1 + 0.2, P0.05; 3.8 + 0.3VS6.3 + 0.4, P0.05.MPO activity: 3.3 + 0.2VS4.7 + 0.2, P0.05; 3.1 + 0.1VS4.9 + 0.2. There is a correlation between the expression of P-JNK protein in the fabric and the degree of lung tissue damage. Conclusion: 1. the hydrogen saturated saline injected into the tail vein has certain protective effect on APALI..2. hydrogen saturated saline may be the protective and therapeutic effect of the JNK cell signaling pathway by its selective antioxidant activity.

【學位授予單位】：瀘州醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R576

【參考文獻】

相關期刊論文 前1條

1 Serge Chooklin;;Pathogenic aspects of pulmonary complications in acute pancreatitis patients[J];Hepatobiliary & Pancreatic Diseases International;2009年02期

本文編號：1800983