■电针(EA)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尚不清楚.这项研究的目的是研究线粒体动力学是否参与EA对脑I/R损伤的影响。
■通过大脑中动脉阻塞/再灌注建立脑I/R损伤的大鼠。随后,电针应用于百会(GV20)和大珠(GV14)穴位,频率为2Hz/5Hz,强度为1.0mA,每次20分钟,一天一次,连续七天。通过改良的神经系统严重程度评分(mNSS)评估治疗结果,2,3,5-三苯基-氯化三唑(TTC)染色,和苏木精-伊红(HE)染色。在透射电镜下观察线粒体形态。使用ELISA评估三磷酸腺苷(ATP)含量和ATP合酶(ATP酶)活性以测量线粒体功能。最后,线粒体动力学相关分子,包括动力蛋白相关蛋白1(Drp1),裂变1(Fis1),mitofusin1(Mfn1),mitofusin2(Mfn2),和视神经萎缩1(OPA1),通过Westernblot和免疫荧光染色进行检测。
■脑I/R损伤引起的神经功能障碍,脑梗死和神经元损伤,所有这些都得到了EA的改善。EA改善了线粒体形态和功能。此外,EA改变了线粒体动力学的平衡。具体来说,数据显示Drp1和Fis1的表达显着降低,导致线粒体裂变的抑制。此外,Mfn1,Mfn2和Opa1与线粒体融合有关,电针治疗后得到有效推广。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,线粒体动力学的平衡对于EA治疗脑I/R损伤至关重要。
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: In summary, our study indicates that the balance of mitochondrial dynamics is crucial for EA therapy to treat cerebral I/R injury.