机构地区:[1]遵义医学院附属医院肝胆胰外科,贵州563000 [2]德阳市人民医院普二科,618000
出 处:《中华实验外科杂志》2014年第7期1511-1513,共3页Chinese Journal of Experimental Surgery
基 金:贵州省科学技术基金资助项目(黔科合J字[2008]2200号)
摘 要:目的 观察Janus激酶2/信号转导与转录激活子3(JAK2/STAT3)信号通路在胰蛋白酶原激活肽(TAP)诱导大鼠胰腺腺泡细胞释放高迁移率族蛋白B1(HMGB1)中的作用。方法 提取大鼠胰腺腺泡细胞,随机分为正常对照组、TAP促进组(终质量浓度为3 nmol/L)、JAK2抑制剂AG490预处理组(25μ.mol/L)、STAT3抑制剂雷帕霉素预处理组(40μg/L),采用聚合酶链反应(PCR)及Western blot法检测3-24 h各组HMGB1 mRNA及蛋白表达水平。结果 与正常对照组HMGB1 mRNA表达水平(1.01±0.04)比较,TAP组6-24 h HMGB1 mRNA表达水平显著增高(2.87±0.08、32.85±1.48、38.43±1.60,P〈0.01),与TAP组比较,AG490预处理组12-24 h HMGB1 mRNA表达均显著抑制(23.40±1.38、19.44±0.89,P〈0.01),与TAP组比较,雷帕霉素预处理组12-24 h HMGB1 mRNA表达均显著抑制(21.14±1.32、17.76±0.57,P〈0.01)。与正常对照组HMGB1蛋白表达水平(0.39±0.02)比较,TAP组3-24 h HMGB1蛋白表达显著增高(0.46±0.02、0.67±0.03、0.72±0.02、0.90±0.03,P〈0.01),与TAP组比较,AG490预处理组12-24 h HMGB1蛋白表达均显著抑制(0.60±0.02、0.54±0.01,P〈0.01),与TAP组比较,雷帕霉素预处理组12-24 h HMGB1蛋白表达均显著抑制(0.59±0.02、0.58±0.01,P〈0.01)。结论 TAP可诱导大鼠胰腺腺泡细胞HMGB1的表达和释放,其机制可能与JAK2/STAT3信号通路有关。Objective To research the effect of Janus activated kinase 2/signal transducer and ac- tivators of transcription 3 ( JAK2/STAT3 ) signaling pathway on the release of high mobility group box 1 ( HMGB1 ) in trypsinogen activation peptide (TAP) -induced rat pancreatic acinar cells. Methods The rat pancreatic acinar cells were isolated, and randomly divided into normal control group, TAP promotion group (3 μmol/L) , AG490 treatment group (25 μmol/L) and RPM treatment group (40 μg/L). Within 3-24 h the HMGB1 mRNA and protein expression levels were detected by using PCR and Western blotting. Results In comparison with the normal control group ( 1.01 ± 0.04), HMGB1 mRNA expression was significantly increased at 6, 12 and 24 h in TAP promotion group (2. 87 ±0. 08, 32. 85 ± 1.48 and 38.43 ± 1.60, P 〈0. 01 for all), that was dramatically inhibited at 12 and 24 h in AG490 treatment group as com pared with TAP promotion group (23.40 ± 1.38 and 19.44 ±0. 89, P 〈0. O1 for all), and that was drmatically inhibited at 12 and 24 h in RPM treatment group as compared with TAP promotion group (21.14 ± 1.32 and 17.76 ± 0.57, P〈 0.01 for all). In comparison with the normal control group (0. 39 ±0. 02), the HMGB1 expression was significantly increased at 3, 6, 12 h and 24 h in TAP promotion group (0. 46 ± 0.02, 0. 67 ± 0. 03, 0. 72 ± 0. 02 and 0. 90 ± 0. 03, P 〈 0. 01 for all), that was dramat-ically inhibited at 12 and 24 h in AG490 treatment group as compared with TAP promotion group (0. 60 ± 0. 02 and 0. 54 ±0. 01, P 〈0. 01 for all), and that was dramatically inhibited at 12 and 24 h in RPM treat ment group as compared with TAP promotion group (0. 59 ± 0.02 and 0. 58 ± 0.01, P 〈 0.01 for all). Conclusion TAP induces rat pancreatic acinar cells to release HMGB1, which is related to intracellular JAK2/STAT3 siznalinz oathwav.
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