Acupuncture protects against cerebral ischemia-reperfusion injury via suppressing endoplasmic reticulum stress-mediated autophagy and apoptosis.

Acupuncture protects against cerebral ischemia-reperfusion injury via suppressing endoplasmic reticulum stress-mediated autophagy and apoptosis.
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针刺通过抑制内质网应激介导的自噬和凋亡来预防脑缺血再灌注损伤

DOI:
10.1186/s10020-020-00236-5
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发表时间:
2020-11-10
期刊:
Molecular medicine (Cambridge, Mass.)
影响因子:
--
通讯作者:
Li H
Li H
中科院分区:
其他
文献类型:
--
作者:
Sun X;Liu H;Sun Z;Zhang B;Wang X;Liu T;Pan T;Gao Y;Jiang X;Li H

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针灸治疗具有神经保护潜力,可减轻脑缺血再灌注(I/R)损伤。内质网(ER)应激被认为参与了脑I/R损伤的发病机制。针灸是否通过调节内质网应激来预防脑I/R损伤仍不清楚。本研究旨在评估内质网应激在针灸对脑I/R损伤的神经保护中的作用及其潜在机制。 通过大脑中动脉闭塞(MCAO)诱导大鼠脑I/R损伤。在再灌注后立即对大鼠的百会(GV 20)和曲鬓(GB7)穴位进行针灸。测定梗死体积、神经功能评分、内质网应激、自噬和细胞凋亡情况。 针灸治疗可减少MCAO大鼠的梗死体积和神经功能评分,并通过使ATF - 6、PERK和IRE1通路失活来抑制内质网应激。由于内质网应激受到抑制,4 - PBA(内质网应激抑制剂)促进了针灸对脑I/R损伤的有益作用。然而,内质网应激激活剂衣霉素显著抵消了针灸的神经保护作用。此外,针灸通过调节MCAO大鼠的内质网应激来抑制自噬。最后,内质网应激参与了针灸对脑I/R损伤中细胞凋亡的神经保护作用。 我们的研究结果表明,针灸对脑I/R损伤具有神经保护作用,这归因于其抑制内质网应激介导的自噬和细胞凋亡。
Acupuncture treatment possesses the neuroprotection potential to attenuate cerebral ischemia–reperfusion (I/R) injury. Endoplasmic reticulum (ER) stress has been suggested to be involved in the pathogenic mechanism of cerebral I/R injury. Whether acupuncture protects against cerebral I/R injury via regulating ER stress remains unclear. This study aimed to evaluate the role of ER stress in the neuroprotection of acupuncture against cerebral I/R injury and its underlying mechanisms. Cerebral I/R injury was induced by middle cerebral artery occlusion (MCAO) in rats. Acupuncture was carried out at Baihui (GV 20), and Qubin (GB7) acupoints in rats immediately after reperfusion. The infarct volumes, neurological score, ER stress, autophagy and apoptosis were determined. Acupuncture treatment decreased infarct volume, neurological score and suppressed ER stress via inactivation of ATF-6, PERK, and IRE1 pathways in MCAO rats. Attributing to ER stress suppression, 4-PBA (ER stress inhibitor) promoted the beneficial effect of acupuncture against cerebral I/R injury. Whereas, ER stress activator tunicamycin significantly counteracted the neuroprotective effects of acupuncture. In addition, acupuncture restrained autophagy via regulating ER stress in MCAO rats. Finally, ER stress took part in the neuroprotective effect of acupuncture against apoptosis in cerebral I/R injury. Our findings suggest that acupuncture offers neuroprotection against cerebral I/R injury, which is attributed to repressing ER stress-mediated autophagy and apoptosis.
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