2020
DOI: 10.1007/s12031-020-01609-5
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Electro-Acupuncture Inhibits p66Shc-Mediated Oxidative Stress to Facilitate Functional Recovery After Spinal Cord Injury

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Cited by 11 publications
(15 citation statements)
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“…Fork-head transcription factor (FoxO) is the key effector of JNK-mediated tumor suppression [ 15 ]. Activation of FoxO regulated by JNK enhances the ability of animals to resist oxidative stress and longevity [ 16 , 17 ]. It has been reported [ 18 ] that fork-head box O3a (FoxO3a) is involved in the myocardial injury process caused by IRI, and the activation of the PI3K/Akt pathway can phosphorylate FoxO3a and transfer it from the nucleus to the cytoplasm to participate in reducing the apoptosis of cardiomyocytes.…”
Section: Introductionmentioning
confidence: 99%
“…Fork-head transcription factor (FoxO) is the key effector of JNK-mediated tumor suppression [ 15 ]. Activation of FoxO regulated by JNK enhances the ability of animals to resist oxidative stress and longevity [ 16 , 17 ]. It has been reported [ 18 ] that fork-head box O3a (FoxO3a) is involved in the myocardial injury process caused by IRI, and the activation of the PI3K/Akt pathway can phosphorylate FoxO3a and transfer it from the nucleus to the cytoplasm to participate in reducing the apoptosis of cardiomyocytes.…”
Section: Introductionmentioning
confidence: 99%
“…Similar to the effect of the reactive oxygen species (ROS) scavenger, acupuncture can inhibit superoxide anion production, decrease JNK/p66Shc-mediated ROS generation, upregulate the apolipoprotein E (ApoE) and nuclear factor E2-related factor 2 (Nrf2)/heme-oxygenase-1 (HO-1) signaling pathways, and reduce the ROS-induced p38MAPK and ERK activation in microglia after SCI ( Choi et al, 2012 ; Dai et al, 2021 ). Notably, the inhibitory effect of electroacupuncture on p38MAPK is significantly enslaved to the acupuncture frequency ( Cheng et al, 2020 ).…”
Section: Mechanism Of Acupuncture Therapy In Spinal Cord Injurymentioning
confidence: 99%
“…87 Deng et al 88 and Lv et al 89 found that EA treatment could up-regulate Nrf2 and its downstream antioxidant molecules hemeoxygenase-1 (HO-1) and glutamate-cysteine ligase modifier subunit (GCLM), and reduce the intensity of neuroinflammation. Cheng et al 90 also showed that EA can alleviate the inflammatory response and promote recovery of myeloid functions by inhibiting the oxidative stress response mediated by p66Shc after SCI. He 91 proposed that EA could reduce the level of NO in the brain of VaD rats and increase the content of superoxide dismutase (SOD), so as to mitigate the level of oxidative stress and the impairment of cognitive function.…”
Section: Mechanism Of Ea-induced Attenuation Of Neuroinflammationmentioning
confidence: 99%
“…87 Deng et al 88 and Lv et al 89 found that EA treatment could up-regulate Nrf2 and its downstream antioxidant molecules hemeoxygenase-1 (HO-1) and glutamate-cysteine ligase modifier subunit (GCLM), and reduce the intensity of neuroinflammation. Cheng et al 90…”
Section: Ea Restrains Damage Secondary To Oxidative Stressmentioning
confidence: 99%