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促血小板生成素对大鼠局灶性脑缺血-再灌注损伤后JAK2/STAT3信号通路的影响

邹成林 陈维钧 孙晓顺 方璟 涂军 赵亚洲

医药导报Issue(8):1019-1023,5.
医药导报Issue(8):1019-1023,5.DOI:10.3870/yydb.2015.08.008

促血小板生成素对大鼠局灶性脑缺血-再灌注损伤后JAK2/STAT3信号通路的影响

Influence of Thrombopoietin on JAK2/STAT3 Signal Transduction Pathway in Focal Cerebral Ischemia-Reperfusion Injury of Rats

邹成林 1陈维钧 1孙晓顺 1方璟 1涂军 1赵亚洲1

作者信息

  • 1. 湖北省荆州市第二人民医院内一科,荆州 434000
  • 折叠

摘要

Abstract

Objective To investigate protective effects of thrombopoietin ( TPO) on cerebral model control in rats and associated signal transduction pathway. Methods Thread embolism was performed to generate cerebral ischemia-reperfusion rat model. Eighty male SD rats were randomly divided into sham operation group, model control group, TPO group, TPO and Janus kinase 2 ( JAK2 ) kinase inhibitor ( AG490 ) group. Before 30 min of ischemia-reperfusion, TPO group was given TPO (5 μg·kg-1) by intraperitoneal injection, TPO + AG490 group was given TPO (5 μg·kg-1) before 30 min of ischemia reperfusion, then given AG490 (8 μg·kg-1), and model control group were given the same dose of 0. 9% sodium chloride solution. The observation time points were 6, 12, 24, and 48 h after ischemia reperfusion. Immunohistochemical staining and Western blotting were used to measure the protein levels of Bcl-2, JAK2 and signal transducer & activator of transcription (STAT3). TdT-mediated dUTP nick end labeling (TUNEL) was used to detect apoptosis. Results Compared with model control group, the number of apoptotic cells were significantly reduced [(67. 50±9. 37) vs. (40. 20±7. 47)], the expression levels of Bcl-2, JAK2 and STAT3 protein were significantly increased [(35. 40±7. 39) vs. (78. 70±9. 75);(35. 68±6. 75) vs. (62.35±7.53); (25.40±9.45) vs.(55.36±9.69), respectively] 24 h after ischeia reperfusion in the TPO group (all P<0. 05). Compared with the TPO group, the Bcl-2, JAK2 and STAT3 protein levels were significantly decreased in TPO and AG490 group [(78. 70±9. 75) vs. (55. 40±9. 35);(62. 35±7. 53) vs. (40. 68±5. 89); (55. 36±9. 69) vs. (30. 40±9. 39), respetively], and the number of apoptotic cells was significantly increased [(40. 20±7. 47) vs. (55. 23±7. 65)] (all P<0. 05). Conclusion TPO can inhibit cell apoptosis after ischemia-reperfusion injury, the mechanism might be related to the activation of JAK2/STAT3 signal transduction pathway through raising the expression of Bcl-2 gene.

关键词

促血小板生成素/大鼠/损伤,缺血-再灌注/细胞凋亡/蛋白质酪氨酸激酶2与转导激活因子3/Bcl-2

Key words

Thrombopoietin/Rats/Injury, ischemia-reperfusion/Apoptosis/Janus kinase 2/signal transducer and activator of transcription/Bcl-2

分类

医药卫生

引用本文复制引用

邹成林,陈维钧,孙晓顺,方璟,涂军,赵亚洲..促血小板生成素对大鼠局灶性脑缺血-再灌注损伤后JAK2/STAT3信号通路的影响[J].医药导报,2015,(8):1019-1023,5.

医药导报

OACSTPCD

1004-0781

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