STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study

钟敦璟; 郭红; 郝嘉; 赵晓晏

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STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study

更新时间：2026-01-09

- STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study
- Journal of Army Medical University Vol. 30, Issue 19, Pages: 1807-1809(2008)
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  CLC： R-332;R329.25;R576.02
- Published：2008
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钟敦璟,郭红,郝嘉,赵晓晏.STAT3对大鼠重症急性胰腺炎血清体外作用AT-ⅡSP-C的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(19):1807-1809.

　ZHONG Dun-jing,GUO Hong,HAO Jia,ZHAO Xiao-yan.STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(19):1807-1809.
钟敦璟,郭红,郝嘉,赵晓晏.STAT3对大鼠重症急性胰腺炎血清体外作用AT-ⅡSP-C的影响[J].陆军军医大学学报(原第三军医大学学报),2008,30(19):1807-1809. DOI：

　ZHONG Dun-jing,GUO Hong,HAO Jia,ZHAO Xiao-yan.STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(19):1807-1809. DOI：

摘要

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-ⅡSP-C表达。结果与对照组比，SAP组STAT3活性增强

STAT3 mRNA表达增强(P0.05)，SP-C 蛋白表达下降(P0.01)；与SAP组比，SAP+AG490组STAT3活性减弱，STAT3mRNA表达减弱(P0.01)，SP-C 蛋白表达下降（P0.01）。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。

Abstract

Objective To study the role of signal transducer and activator of transcription3 (Stat3) in alveolar type Ⅱ epithelial cells (AT-Ⅱ) treated with the serum from rat model of severe acute pancreatitis. Methods AT-Ⅱ cells of primary culture were treated with serum from rat model of severe acute pancreatitis (SAP group)

or SAP serum+AG490 (JAK inhibitor)

while the normal cell control was set. AT-Ⅱ cells after treatment were collected to determine activation of Stat3 by EMSA

Stat3 mRNA expression by RT-PCR

and surfactant protein C (SP-C) level in AT-Ⅱ cells by flow cytometry. Results Stat3 protein and mRNA levels were enhanced in SAP group (P0.05)

whereas SP-C protein level declined (P0.01)

compared with control cells. Compared with SAP group

Stat3 protein and mRNA levels decreased and SP-C protein level declined after the cells were treated with SAP serum+AG490 (P0.01). Conclusion JAK/STAT pathway is involved in the pathogenesis of AT-Ⅱ cell injury in severe acute pancreatitis.

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