Non-invasive remote limb ischemic postconditioning protects rats against focal cerebral ischemia by upregulating STAT3 and reducing apoptosis.
Non-invasive remote limb ischemic postconditioning protects rats against focal cerebral ischemia by upregulating STAT3 and reducing apoptosis.
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DOI：
10.3892/ijmm.2014.1873
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发表时间：
2014-10
影响因子：
5.4
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Cheng Z;Li L;Mo X;Zhang L;Xie Y;Guo Q;Wang Y
信号转导子和转录激活子3（STAT 3）信号通路参与细胞凋亡和炎症过程。缺血预处理（IPC）和缺血后处理（IPTC）抑制这两个过程。在本研究中，我们使用经典的大鼠局灶性脑缺血模型，研究了磷酸化STAT 3（p-STAT 3）介导的细胞凋亡和炎症在非侵入性远端肢体IPTC（NRI）后的作用。将45只成年雄性SD大鼠随机分为假手术组、缺血再灌注组（I/R组）和NRI组，每组15只。在再灌注开始时实施NRI 40。于脑再灌注24 h后进行神经功能缺损评分（NDS）、脑梗死面积、脑组织形态学及神经细胞凋亡检测。Western blot检测半暗带区Bcl-2、Bax、核因子-κB（NF-κB）、肿瘤坏死因子-α（TNF-α）和p-STAT 3蛋白表达水平。与假手术组相比，I/R组脑梗死体积、凋亡细胞数及Bcl-2、Bax、NF-κB和TNF-α蛋白表达均增加。然而，与I/R组相比，NRI组的这些水平降低。I/R组半暗带区凋亡细胞数较NRI组和假手术组增多。与假手术组和I/R组相比，NRI组p-STAT 3蛋白表达增加。这些结果表明，NRI对脑I/R损伤的保护作用可能与通过激活STAT 3减轻神经元凋亡和炎症有关。
The signal transducer and activator of transcription 3 (STAT3) signaling pathway has been implicated in cell apoptosis and inflammatory processes. Ischemic preconditioning (IPC) and ischemic postconditioning (IPTC) inhibit both of these processes. In the present study, we investigated the role of phosphorylated STAT3 (p-STAT3)-mediated apoptosis and inflammation following non-invasive remote limb IPTC (NRIPoC) using a classic rat model of focal cerebral ischemia. Forty-five adult male Sprague-Dawley rats were divided randomly into 3 groups (n=15 per group): the sham-operated, ischemia/reperfusion (I/R) and NRIPoC groups. NRIPoC was implemented at the beginning of reperfusion. At 24 h after cerebral reperfusion, we evaluated the neurological deficit score (NDS), assessed the cerebral infarct size and tissue morphology, and evaluated neuronal apoptosis. The protein expression levels of Bcl-2, Bax, nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α) and p-STAT3 in the penumbra region were assessed by western blot analysis. The cerebral infarct volume, the number of apoptotic cells and the protein expression levels of Bcl-2, Bax, NF-κB and TNF-α were all found to be increased in the I/R group compared with the sham-operated group. However, these levels were decreased in the NRIPoC group compared with the I/R group. The number of apoptotic cells in the penumbra in the I/R group was increased compared with that in the NRIPoC and sham-operated groups. The protein expression of p-STAT3 was increased in the NRIPoC group compared with the sham-operated and I/R groups. These results indicate that the protective effects of NRIPoC against cerebral I/R injury may be related to the attenuation of neuronal apoptosis and inflammation through the activation of STAT3.
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影响因子：
3.3
作者：
Hong, Deok Man;Jeon, Yunseok;Hwang, Ho Young
通讯作者：
Hwang, Ho Young
影响因子：
6.4
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2.2
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影响因子：
14.5
作者：
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2.5
作者：
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通讯作者：
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