Isoflurane post-conditioning contributes to anti-apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway.
Isoflurane post-conditioning contributes to anti-apoptotic effect after cerebral ischaemia in rats through the ERK5/MEF2D signaling pathway.
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异氟烷后处理通过ERK5/MEF2D信号通路发挥大鼠脑缺血后的抗凋亡作用
DOI：
10.1111/jcmm.16282
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发表时间：
2021-04
影响因子：
5.3
通讯作者：
Wang S
中科院分区：
文献类型：
--
作者：
Zhang Q;Yin J;Xu F;Zhai J;Yin J;Ge M;Zhou W;Li N;Qin X;Li Y;Wang S
异氟醚(ISO)后处理诱导的脑缺血再灌注损伤的脑保护机制尚不清楚。心肌细胞增强因子2(MEF2D)在多种模型中被证明可以促进神经存活，在这些模型中，多个生存和死亡信号汇聚在MEF2D上并调节其活性。在此，我们研究了MEF2D对ISO后处理对大鼠脑缺血/再灌注(I/R)损伤后神经保护作用的影响。大鼠接受大脑中动脉闭塞(MCAO)手术，缺血90分钟，再灌注24-48小时。MCAO后12、24、48h采用改良神经严重度评分(MNSS)评定神经功能状态。采用被动回避试验(PAT)评定认知功能。分别用HE染色和Nissl‘s染色进行组织学和神经病理学评价。免疫荧光染色、Western blotting和TUNEL染色检测MEF2D、ERK5、GFAP和caspase-3的表达，以评估海马CA1区细胞凋亡的严重程度。我们发现MEF2D参与了脑I/R损伤后的神经保护作用，ISO的后处理显著促进ERK5的磷酸化，增加MEF2D的转录活性，抑制caspase-3的表达，起到脑保护作用。
The mechanisms of brain protection during ischaemic reperfusion injury induced by isoflurane (ISO) post‐conditioning are unclear. Myocyte enhancement factor 2 (MEF2D) has been shown to promote neural survival in a variety of models, in which multiple survival and death signals converge on MEF2D and modulate its activity. Here, we investigated the effect of MEF2D on the neuroprotective effects of ISO post‐conditioning on rats after cerebral ischaemia/reperfusion (I/R) injury. Rats underwent middle cerebral artery occlusion (MCAO) surgery with ischaemia for 90 minutes and reperfusion for 24‐48 hours. After MCAO, neurological status was assessed at 12, 24 and 48 hours by the Modified Neurological Severity Score (mNSS) test. The passive avoidance test (PAT) was used to assess cognition function. Histological and neuropathological evaluations were performed with HE staining and Nissl's staining, respectively. We measured the expression of MEF2D, ERK5, GFAP and caspase‐3 by immunofluorescent staining and Western blotting, and TUNEL staining to assess the severity of apoptosis in hippocampal CA1 area. We found that MEF2D was involved in nerve protection after I/R injury, and post‐treatment of ISO significantly promoted the phosphorylation of ERK5, increased MEF2D transcriptional activity, inhibited the expression of caspase‐3 and played a role of brain protection.
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MEF2D 介导亚甲蓝对 HT22 海马细胞中谷氨酸诱导的氧化损伤的神经保护作用
影响因子：
5.1
作者：
Chen, Zi-wei;Liu, Anmin;Pi, Rong-biao
通讯作者：
Pi, Rong-biao
影响因子：
3.6
作者：
Cheon SY;Kim SY;Kam EH;Lee JH;Kim JM;Kim EJ;Kim TW;Koo BN
通讯作者：
Koo BN
DOI：
10.3390/molecules23071788
发表时间：
2018-07-20
期刊：
Molecules (Basel, Switzerland)
影响因子：
--
作者：
Cui HX;Chen JH;Li JW;Cheng FR;Yuan K
通讯作者：
Yuan K
影响因子：
8.8
作者：
Bickler, PE;Zhan, XH;Fahlman, CS
通讯作者：
Fahlman, CS
影响因子：
5.3
作者：
Kasler, HG;Victoria, J;Winoto, A
通讯作者：
Winoto, A