Li Cheng-Long, Mao Wei, Zhang Li-da, Ji Hai-Sheng, Tong Ting-Ting, Wang Jun-Li, Wu Xiao-Qing, Li Kui-Wu, Wu Hai-Yang, Zhang Guo-Qing, Zhang Jun-Yu, Han Wei, Wang Ying
First Affiliated Hospital (First Clinical Medical College) of Anhui University of Chinese Medicine, Hefei, 230012, Anhui, China.
Brain Hospital Affiliated to Guangzhou Medical University, Guangzhou, 510370, Guangdong, China.
Heliyon. 2024 Jul 19;10(14):e34986. doi: 10.1016/j.heliyon.2024.e34986. eCollection 2024 Jul 30.
Electroacupuncture (EA) has been shown to promote functional recovery after cerebral ischemia-reperfusion (I/R) injury. However, the contribution of mitochondrial dynamics to recovery remains unclear. The aim of this study was to investigate whether mitochondrial dynamics are involved in the effects of EA on cerebral I/R injury.
The rats with cerebral I/R injury were established by the middle cerebral artery occlusion/reperfusion. Subsequently, EA was applied to Baihui (GV20) and Dazhui (GV14) acupoints, with 2 Hz/5 Hz in frequency, 1.0 mA in intensity, 20 min each time, once a day for seven consecutive days. The therapeutic outcomes were assessed by modified neurological severity score (mNSS), 2,3,5-Triphenyte-trazolium chloride (TTC) staining, and hematoxylin-eosin (HE) staining. Mitochondrial morphology was observed under transmission electron microscopy. Adenosine triphosphate (ATP) content and ATP synthases (ATPases) activity were evaluated to measure mitochondrial function using ELISA. Finally, mitochondrial dynamics-related molecules, including dynamin-related protein 1 (Drp1), fission 1 (Fis1), mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and optic atrophy 1 (OPA1), were detected by Western blot and immunofluorescence staining.
Cerebral I/R injury induced neurological dysfunction, cerebral infarction and neuronal injury, all of which were ameliorated by EA And EA improved mitochondrial morphology and function. Moreover, EA altered the balance of mitochondrial dynamics. Specifically, the data showed a significant decrease in the expression of Drp1 and Fis1, leading to the inhibition of mitochondrial fission. Additionally, Mfn1, Mfn2 and Opa1, which are related to mitochondrial fusion, were effectively promoted after EA treatment. However, sham EA did not show any neuroprotective effects in rats with cerebral I/R injury.
In summary, our study indicates that the balance of mitochondrial dynamics is crucial for EA therapy to treat cerebral I/R injury.
电针已被证明可促进脑缺血再灌注（I/R）损伤后的功能恢复。然而，线粒体动力学对恢复的贡献仍不清楚。本研究的目的是探讨线粒体动力学是否参与电针对脑I/R损伤的影响。
采用大脑中动脉闭塞/再灌注法建立脑I/R损伤大鼠模型。随后，将电针应用于百会（GV20）和大椎（GV14）穴位，频率为2Hz/5Hz，强度为1.0mA，每次20分钟，每天一次，连续七天。通过改良神经功能缺损评分（mNSS）、2,3,5-氯化三苯基四氮唑（TTC）染色和苏木精-伊红（HE）染色评估治疗效果。在透射电子显微镜下观察线粒体形态。使用酶联免疫吸附测定（ELISA）评估三磷酸腺苷（ATP）含量和ATP合酶（ATPases）活性以测量线粒体功能。最后，通过蛋白质免疫印迹法（Western blot）和免疫荧光染色检测与线粒体动力学相关的分子，包括动力相关蛋白1（Drp1）、裂变蛋白1（Fis1）、线粒体融合蛋白1（Mfn1）、线粒体融合蛋白2（Mfn2）和视神经萎缩蛋白1（OPA1）。
脑I/R损伤导致神经功能障碍、脑梗死和神经元损伤，而电针均可改善这些情况。电针还改善了线粒体形态和功能。此外，电针改变了线粒体动力学的平衡。具体而言，数据显示Drp1和Fis1的表达显著降低，导致线粒体裂变受到抑制。此外，电针治疗后，与线粒体融合相关的Mfn1、Mfn2和Opa1得到有效促进。然而，假电针对脑I/R损伤大鼠未显示任何神经保护作用。
总之，我们的研究表明，线粒体动力学平衡对于电针治疗脑I/R损伤至关重要。
