Electroacupuncture Pretreatment against Cerebral Ischemia/Reperfusion Injury through Mitophagy

Mao, Chenlu; Hu, Cheng; Zhou, Yudi; Zou, Rong; Li, Sha; Cui, Yaomei; Tian, Weiqian

doi:10.1155/2020/7486041

Cited by 19 publications

(15 citation statements)

References 24 publications

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“…According to our current knowledge, the concept of "EA pretreatment" was rst proposed in 2003, indicating that pretreatment with repeated EA at Baihui acupoint (GV20) attenuated transient focal cerebral ischemic injury in MCAO rats [21]. Besides GV20 [22], EA pretreatment in CIRI or ischemic stroke is always associated with acupuncture prescriptions of single acupoint or acupoints combination, such as Shuigou (GV26) [23], Sanyinjiao (SP6), Neiguan (PC6) [24], Dazhui (GV14) [25], Zusanli (ST36), and Quchi (LI11) [26], etc. Although the neuroprotective effect of EA pretreatment has been widely reported and con rmed, there is currently no uniform standard for the selection and combination of acupoints because of the complicated issues, such as acupoint indications, clinical syndrome differentiation, and individualization of treatment.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Pretreatment Attenuates Cerebral Ischemia-Reperfusion Injury through Transient Receptor Potential Vanilloid 1-Mediated Anti-Apoptosis via Inhibiting NF-kB Signaling Pathway

Yin¹,

Long²,

Wang³

et al. 2021

Preprint

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Our previous study showed that electroacupuncture (EA) pretreatment elicited protective effect on cerebral ischemia-reperfusion injury in rats, at least partly, which was associated with transient receptor potential vanilloid 1 (TRPV1)-regulated anti-oxidant stress and anti-inflammation. In this study, we further investigated the possible contribution of TRPV1-mediated anti-apoptosis in EA pretreatment-evoked neuroprotection. After EA pretreatment at Baihui (GV20), bilateral Shenshu (BL23) and Sanyinjiao (SP6) acupoints, transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 6 h in rats. Then, infarct volume, nerve cell injury, neuronal apoptosis, NF-κB signaling activation, and expression of TRPV1 were evaluated by TTC staining, hematoxylin-eosin staining, transmission electron microscopy, immunochemistry, immunofluorescence, and Western blot, respectively. The presented data showed that EA pretreatment significantly reduced infarct volume, relieved nerve cell injury, decreased the expression of pro-apoptotic proteins Bax and cleaved caspase-3, increased the level of anti-apoptotic protein Bcl-2, inhibited NF-κB (p65) transcriptional activity, and curbed TRPV1 expression in MCAO rats. By contrast, enhancement of TRPV1 expression accompanying capsaicin application, the specific TRPV1 agonists, markedly accelerated nerve cell damage, aggravated neuronal apoptosis, prompted nuclear translocation of NF-κB (p65), resulting in the reversion of EA pretreatment-evoked neuroprotective effect in MCAO rats. Thus, we conclude that EA pretreatment-induced downregulation of neuronal TRPV1 expression plays an anti-apoptosis role through inhibiting NF-κB signaling pathway, thereby protecting MCAO rats from cerebral ischemia-reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture Pretreatment Attenuates Cerebral Ischemia-Reperfusion Injury through Transient Receptor Potential Vanilloid 1-Mediated Anti-Apoptosis via Inhibiting NF-kB Signaling Pathway

Yin¹,

Long²,

Wang³

et al. 2021

Preprint

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“…Later, Mao et al (2020) also found EA pretreatment has a protective effect on cerebral I/R injury through promoting mitophagy, based on the results that the number of autophagosomes, FUNDC1, p62, and the ratio of LC3-II/I were significantly increased. Still, mitochondrial membrane potential and autophagy-related protein p-mTORC1 significantly decreased in the I/R group (Mao et al, 2020). He et al (2019) showed that ATF4 overexpression induced by AAV was protective against cerebral I/R injury by upregulating Parkin expression, enhance mitophagy activity and inhibit NLRP3 inflammasome-mediated inflammatory response.…”

Section: Therapeutic Potential Of Mitophagy Regulation In I/r Injurymentioning

confidence: 97%

Section: Mitophagy In I/r Injurymentioning

confidence: 97%

“…Recently, Wang et al (2019) demonstrated that EA ameliorates nitro/oxidative stress-induced mitochondrial functional damage and reduces the accumulation of damaged mitochondria via Pink1/Parkin-mediated mitophagy clearance to protect cells against neuronal injury in cerebral I/R. Later, Mao et al (2020) also found EA pretreatment has a protective effect on cerebral I/R injury through promoting mitophagy, based on the results that the number of autophagosomes, FUNDC1, p62, and the ratio of LC3-II/I were significantly increased. Still, mitochondrial membrane potential and autophagy-related protein p-mTORC1 significantly decreased in the I/R group ( Mao et al, 2020 ).…”

Section: Mitophagy In I/r Injurymentioning

confidence: 99%

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Mitophagy in Cerebral Ischemia and Ischemia/Reperfusion Injury

Shen

Gan

Yang

et al. 2021

Front. Aging Neurosci.

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Ischemic stroke is a severe cerebrovascular disease with high mortality and morbidity. In recent years, reperfusion treatments based on thrombolytic and thrombectomy are major managements for ischemic stroke patients, and the recanalization time window has been extended to over 24 h. However, with the extension of the time window, the risk of ischemia/reperfusion (I/R) injury following reperfusion therapy becomes a big challenge for patient outcomes. I/R injury leads to neuronal death due to the imbalance in metabolic supply and demand, which is usually related to mitochondrial dysfunction. Mitophagy is a type of selective autophagy referring to the process of specific autophagic elimination of damaged or dysfunctional mitochondria to prevent the generation of excessive reactive oxygen species (ROS) and the subsequent cell death. Recent advances have implicated the protective role of mitophagy in cerebral ischemia is mainly associated with its neuroprotective effects in I/R injury. This review discusses the involvement of mitochondria dynamics and mitophagy in the pathophysiology of ischemic stroke and I/R injury in particular, focusing on the therapeutic potential of mitophagy regulation and the possibility of using mitophagy-related interventions as an adjunctive approach for neuroprotective time window extension after ischemic stroke.

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“…For example, electroacupuncture preconditioning has a protective effect in patients undergoing heart valve replacement surgery, and this is caused by inhibition of mitophagy mediated by the mTORC1-ULK1-FUNDC1 pathway (Xiao et al, 2020). The protective effect of electroacupuncture pretreatment on cerebral I/R injury also correlates with p-mTORC1 mitophagy (Mao et al, 2020). Moreover, the transient receptor potential cation channel subfamily V member 1 (TRPV1) factor alleviates I/R-induced acute renal injury (Wei et al, 2020).…”

Section: Hypoxia and I/rmentioning

confidence: 98%

FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

Shao

et al. 2021

Front. Cell Dev. Biol.

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Mitochondrial autophagy (or mitophagy) regulates the mitochondrial network and function to contribute to multiple cellular processes. The protective effect of homeostatic mitophagy in cardiovascular diseases (CVDs) has attracted increasing attention. FUN14 domain containing 1 (FUNDC1), an identified mitophagy receptor, plays an essential role in CVDs. Different expression levels of FUNDC1 and its phosphorylated state at different sites alleviate or exacerbate hypoxia and ischemia/reperfusion injury, cardiac hypertrophy, or metabolic damage through promotion or inhibition of mitophagy. In addition, FUNDC1 can be enriched at contact sites between mitochondria and the endoplasmic reticulum (ER), determining the formation of mitochondria-associated membranes (MAMs) that regulate cellular calcium (Ca2+) homeostasis and mitochondrial dynamics to prevent heart dysfunction. Moreover, FUNDC1 has also been involved in inflammatory cardiac diseases such as septic cardiomyopathy. In this review, we collect and summarize the evidence on the roles of FUNDC1 exclusively in various CVDs, describing its interactions with different cellular organelles, its involvement in multiple cellular processes, and its associated signaling pathways. FUNDC1 may become a promising therapeutic target for the prevention and management of various CVDs.

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Electroacupuncture Pretreatment against Cerebral Ischemia/Reperfusion Injury through Mitophagy

Cited by 19 publications

References 24 publications

Electroacupuncture Pretreatment Attenuates Cerebral Ischemia-Reperfusion Injury through Transient Receptor Potential Vanilloid 1-Mediated Anti-Apoptosis via Inhibiting NF-kB Signaling Pathway

Electroacupuncture Pretreatment Attenuates Cerebral Ischemia-Reperfusion Injury through Transient Receptor Potential Vanilloid 1-Mediated Anti-Apoptosis via Inhibiting NF-kB Signaling Pathway

Mitophagy in Cerebral Ischemia and Ischemia/Reperfusion Injury

FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

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