[1]钟敦璟,郭红,郝嘉,等.STAT3对大鼠重症急性胰腺炎血清体外作用AT-ⅡSP-C的影响[J].第三军医大学学报,2008,30(19):1807-1809.
 ZHONG Dun-jing,GUO Hong,HAO Jia,et al.STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study[J].J Third Mil Med Univ,2008,30(19):1807-1809.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
30卷
期数:
2008年第19期
页码:
1807-1809
栏目:
论著
出版日期:
2008-10-10

文章信息/Info

Title:
STAT3 participates in the injury of alveolar type Ⅱ epithelial cells during severe acute pancreatitis: an in vitro study
作者:
钟敦璟郭红郝嘉赵晓晏
第三军医大学新桥医院:消化内科,全军心血管外科中心
Author(s):
ZHONG Dun-jing GUO Hong HAO Jia ZHAO Xiao-yan
Department of Gastroenterology, Cardiovascular Disease Research Center, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China
关键词:
STAT3重症急性胰腺炎AT-ⅡSP-C
Keywords:
STAT3 severe acute pancreatitis alveolar type Ⅱ epithelial cells surfactant protein C
分类号:
R-332; R329.25; R576.02
文献标志码:
A
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(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,STAT3mRNA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。
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 (P<0.05), whereas SP-C protein level declined (P<0.01), 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 (P<0.01).     Conclusion    JAK/STAT pathway is involved in the pathogenesis of AT-Ⅱ cell injury in severe acute pancreatitis.

参考文献/References:

钟敦璟,郭红,郝嘉,等. STAT3对大鼠重症急性胰腺炎血清体外作用AT-ⅡSP-C的影响[J]. 第三军医大学学报, 2008, 30(19):1807-1809.

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更新日期/Last Update: 2008-09-26