Abstract
Cerebral ischemia/reperfusion (I/R) injury can induce the mitophagy of neurons in the ischemic brain. Electroacupuncture (EA) pretreatment has a protective effect on cerebral ischemia/reperfusion injury. However, its internal mechanism still needs to be further studied. The present study's purpose is to investigate whether mitophagy is involved in neuroprotection elicited by EA pretreatment in a rat model of cerebral ischemia/reperfusion injury. The rats were pretreated with vehicle, EA at the Baihui (GV20) and Shuigou (GV26) acupoints 30 min daily, for 5 days consecutively prior to the focal cerebral ischemia injury induced by the middle cerebral artery occlusion (MCAO) model. Compared to the sham group, the neurological scores, infarction volume, number of autophagosomes, FUNDC1, p62, and the ratio of LC3-II/I were significantly increased but mitochondrial membrane potential and autophagy-related protein p-mTORC1 significantly decreased in the I/R group. However, EA pretreatment significantly reversed these trends. Overall, the results of this study demonstrated that EA pretreatment protected the cerebral ischemia/reperfusion injury which maybe correlated with mitophagy.
Highlights
As an important alternative therapy, electroacupuncture (EA) is being accepted by more and more countries and regions
FUNDC1 is an integral mitochondrial outer-membrane protein and a receptor of hypoxia-induced mitophagy. e FUNDC1 contains three transmembrane domains and N-terminal LC3 interaction region, which plays an important role in mitochondrial autophagy [14]
It can interact with LC3 through its typical LC3-binding motif Y 【18】 xxL 【21】, and mutation of the LC3-interaction region impaired its interaction with LC3 and the subsequent induction of mitophagy [15]
Summary
As an important alternative therapy, electroacupuncture (EA) is being accepted by more and more countries and regions. After cerebral I/R injury, autophagy is significantly activated, which is manifested as autophagy of cytoplasm and mitochondria, aggravating neuron damage [5]. EA can improve the energy metabolism of mitochondria and reduce or reverse the damage of neurons after cerebral I/R in rats, which has a good neuroprotective effect [13].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Evidence-Based Complementary and Alternative Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
