电针预处理通过抑制乳酸生成及其衍生蛋白乳酸化形成减少缺血性脑损伤。

IF 4.8 1区 医学 Q1 NEUROSCIENCES CNS Neuroscience & Therapeutics Pub Date : 2025-01-20 DOI:10.1111/cns.70231
Xin-Ru Pan, Yao-Dan Zhang, Yuan-Hui Gan, Jia-Hang Zhang, Su-Jin Gao, Xiao-Shuang Feng, Jia-Xin Xie, Yu-Fei Wang, Xin-Xiao Zhang, Peng-Fei Wang, Shu-Guang Yu, Yong Tang, Xiao-Yi Xiong
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引用次数: 0

摘要

目的:鉴于电针(EA)预处理抑制乳酸生成,乳酸源性赖氨酸泌乳(Kla)加重缺血性脑损伤,我们旨在探讨Kla蛋白的形成是否参与电针预处理对缺血性脑损伤的缓解作用。方法:在C57BL/6J雄性小鼠永久性大脑中动脉闭塞(pMCAO)手术前,对其百会穴(GV20)进行电刺激。采用Western blot和免疫荧光染色法观察神经元存活、星形胶质细胞活化、蛋白Kla水平,并用商品化试剂盒检测缺血脑组织乳酸水平。采用TTC染色和神经功能评分评价小鼠脑损伤。结果:我们发现EA预处理后小鼠缺血脑组织乳酸含量和蛋白Kla水平明显降低,并伴有星形胶质细胞活化和神经元损伤死亡的减少。同时,我们发现EA预处理能有效逆转乳酸补充引起的缺血性脑损伤恶化。然而,EA预处理并没有进一步降低糖酵解抑制后缺血性脑卒中小鼠的乳酸含量和蛋白Kla水平,也没有改善脑损伤。结论:我们的研究表明,EA预处理通过抑制缺血性脑卒中小鼠乳酸生成及其衍生蛋白Kla的形成来减轻缺血性脑损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Electroacupuncture Pretreatment Reduces Ischemic Brain Injury by Inhibiting the Lactate Production and Its Derived Protein Lactylation Formation

Aim

Given that electroacupuncture (EA) pretreatment inhibits lactate production and lactate-derived lysine lactation (Kla) aggravates ischemic brain injury, we aimed to investigate whether the formation of Kla protein is involved in EA pretreatment to alleviate ischemic brain injury.

Methods

EA was performed on the Baihui acupoint (GV20) of male C57BL/6J mice before receiving the permanent middle cerebral artery occlusion (pMCAO) surgery. Western blot and immunofluorescent staining were used to observe neuronal survival, astrocyte activation, and protein Kla levels, and the lactate levels in ischemic brains were assayed with a commercial kit. TTC staining and neurological function scores are performed to evaluate the brain damage in mice.

Results

We found that the increased lactate content and protein Kla levels were significantly decreased in ischemic brain tissue of mice after receiving EA pretreatment, and accompanied by the reduction of astrocyte activation and neuronal injury and death. Meantime, we found that EA pretreatment was effective in reversing the worsening of ischemic brain injury caused by lactate supplementation. However, EA pretreatment did not further reduce the lactate content and protein Kla levels and ameliorate brain injury in ischemic stroke mice after inhibition of glycolysis.

Conclusion

Our study reveals that EA pretreatment reduced ischemic brain damage by inhibiting lactate production and its derived protein Kla formation in mice with ischemic stroke.

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来源期刊
CNS Neuroscience & Therapeutics
CNS Neuroscience & Therapeutics 医学-神经科学
CiteScore
7.30
自引率
12.70%
发文量
240
审稿时长
2 months
期刊介绍: CNS Neuroscience & Therapeutics provides a medium for rapid publication of original clinical, experimental, and translational research papers, timely reviews and reports of novel findings of therapeutic relevance to the central nervous system, as well as papers related to clinical pharmacology, drug development and novel methodologies for drug evaluation. The journal focuses on neurological and psychiatric diseases such as stroke, Parkinson’s disease, Alzheimer’s disease, depression, schizophrenia, epilepsy, and drug abuse.
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