论文部分内容阅读
目的探讨信号转导-转录活化因子3(Stat3)信号通路在大鼠重症急性胰腺炎血清体外作用于肺泡Ⅱ型上皮细胞(AT-Ⅱ)的影响。方法原代培养肺泡Ⅱ型上皮细胞分成:①对照组:加入不含大鼠胰腺炎血清的DMEM培养液的正常AT-Ⅱ;②SAP组:加入含大鼠胰腺炎血清的DMEM培养液的正常AT-Ⅱ;③SAP+AG490组:用AG490预处理细胞,加入含大鼠胰腺炎血清的DMEM培养液的正常AT-Ⅱ。EMSA法测STAT3活化状态;RT-PCR检测mRNA水平;流式细胞技术检测AT-Ⅱ SP-C表达。结果与对照组比,SAP组STAT3活性增强,STAT3 mRNA表达增强(P<0.05),SP-C蛋白表达下降(P<0.01);与SAP组比,SAP+AG490组STAT3活性减弱,STAT3 mRNA表达减弱(P<0.01),SP-C蛋白表达下降(P<0.01)。结论JAK激酶/转录信号传导和激活因子3(Stat3)信号传导通路参与重症急性胰腺炎中AT-Ⅱ的损伤的病理生理过程。
Objective To investigate the effect of signal transducers and activators of transcription 3 (STAT3) signaling pathway on alveolar type Ⅱ epithelial cells (AT-Ⅱ) in serum of severe acute pancreatitis in rats. Methods Primary culture of alveolar type Ⅱ epithelial cells was divided into: ① control group: normal AT-Ⅱ in DMEM medium without rat pancreatitis serum; ② SAP group: normal AT with DMEM medium containing rat pancreatitis -Ⅱ; ③SAP + AG490 group: Cells were pretreated with AG490, and normal AT-Ⅱ in DMEM culture medium containing rat pancreatitis was added. The STAT3 activation status was measured by EMSA, the mRNA level was detected by RT-PCR and the expression of AT-Ⅱ SP-C was detected by flow cytometry. Results Compared with the control group, STAT3 activity in SAP group was increased, STAT3 mRNA expression was increased (P <0.05) and SP-C protein expression was decreased in SAP group (P <0.01) (P <0.01), the expression of SP-C protein decreased (P <0.01). Conclusions JAK kinase / STAT3 signal transduction pathway is involved in the pathophysiological process of AT-Ⅱ injury in severe acute pancreatitis.