Effect of Acupuncture on Oxidative Stress Induced by Cerebral Ischemia-Reperfusion Injury

Chen, Chao Hsien; Hsieh, Ching Liang

doi:10.3390/antiox9030248

Cited by 33 publications

(29 citation statements)

References 58 publications

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“…MDA is the terminal production of lipid peroxidation and used to measure the level of lipid peroxidation [ 20 ]. As mentioned, SOD and GHSPx are two antioxidant enzymes [ 7 ]. Results of this study have manifested that miR-380-5p inhibited MDA level and increased SOD and GHSPx levels, suggesting that miR-380-5p played an antioxidant role in CIR injury, which prevented neuronal cell injury induced by OGD/R.…”

Section: Discussionmentioning

confidence: 99%

“…During cerebral ischemia, the blood supply to brain was reduced, which led to the reduction of oxygen and glucose supply to the affected brain tissue [ 6 ]. Aerobic metabolism promoted the abundance of reactive oxygen species (ROS), a type of free radical, which contributed to cell necrosis and death lipid peroxidation [ 7 ]. In normal condition, ROS can be scavenged by superoxide dismutase (SOD), the most crucial antioxidant enzyme in brain [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…In normal condition, ROS can be scavenged by superoxide dismutase (SOD), the most crucial antioxidant enzyme in brain [ 8 ]. SOD can convert into H 2 O 2 , and further into H 2 O and O 2 by glutathione peroxidase (GSHPx) [ 7 , 9 ]. Therefore, increase of SOD and GSHPx activity could prevent cell death during CIR injury.…”

Section: Introductionmentioning

confidence: 99%

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miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

Wang

2021

Translational Neuroscience

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Background This study aimed to explore the role of miR-380-5p in cerebral ischemia/reperfusion (CIR) injury-induced neuronal cell death and the potential signaling pathway involved. Methodology Human neuroblastoma cell line SH-SY5Y cells were used in this study. Oxygen and glucose deprivation/reperfusion (OGD/R) model was used to mimic ischemia/reperfusion injury. CCK-8 assay and flow cytometry were used to examine cell survival. Quantitative real time PCR (RT-qPCR) assay and Western blotting were used to measure the change of RNA and protein expression, respectively. TargetScan and Luciferase assay was used to confirm the target of miR-380-5p. Malondialdehyde (MDA) superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) were measured using commercial kits. Results miR-380-5p was downregulated in SH-SY5Y cells after OGD/R. Cell viability was increased by miR-380-5p, while cell apoptosis was reduced by miR-380-5p mimics. MDA was reduced by miR-380-5p mimics, while SOD and GSHPx were increased by miR-380-5p. Results of TargetScan and luciferase assay have showed that BACH1 is the direct target of miR-380-5p. Expression of NRF2 was upregulated after OGD/R, but was not affected by miR-380-5p. mRNA expression of HO-1 and NQO1 and ARE activity were increased by miR-380-5p. Overexpression of BACH1 reversed the antioxidant and neuroprotective effects of miR-380-5p. Conclusion miR-380-5p inhibited cell death induced by CIR injury through target BACH1 which also facilitated the activation of NRF2, indicating the antioxidant and neuroprotective effects of miR-380-5p.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

Wang

2021

Translational Neuroscience

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“…SOD is the most crucial antioxidant enzyme. [ 64 ] It catalyzes the dismutation of superoxide anion free radical (O 2 - ) into molecular oxygen and hydrogen peroxide (H 2 O 2 ), and decrease the O 2 - level which damages the cells at excessive concentration. [ 65 ] The decrease in SOD level indicates aging.…”

Section: Discussionmentioning

confidence: 99%

The effect of scalp electroacupuncture combined with Memantine in patients with vascular dementia

et al. 2020

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“…The most effective treatment for AIS is intravascular recanalization within a certain time window ( 3 - 5 ). Recanalization following AIS is likely to cause cerebral ischemia-reperfusion injury (CIRI), during which excess free radicals attack cells in the tissues that regain blood supply ( 6 , 7 ). CIRI leads to neuronal cell necrosis and apoptosis through a series of pathological processes, such as energy metabolism disorders, excitotoxicity, neuroinflammation, oxidative damage and calcium overload ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV attenuates cerebral ischemia‑reperfusion injury in rats through the inhibition of calcium‑sensing receptor‑mediated apoptosis

Zhang

Zhao

et al. 2020

Int J Mol Med

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cerebral ischemia-reperfusion injury (cIRI), caused by the reperfusion of blocked vessels following ischemic stroke, can lead to secondary brain injury. Throughout cIRI, apoptosis serves an important role. Astragaloside IV is a potential neuroprotectant that alleviates cIRI by inhibiting apoptosis. The calcium-sensing receptor (caSR) is a G-protein-coupled receptor, the activation of which aggravates ischemia-reperfusion injury. The aim of the present study was to investigate whether the protective effect of Astragaloside IV on cIRI may be associated with the regulation of caSR. A rat middle cerebral artery occlusion/reperfusion (McAO/R) model and an oxygen and glucose deprivation/reoxygenation (OGd/R) model of pheochromocytoma (Pc12) cells were used to study the neuronal injury induced by cIRI. Neurological function scores (NFS), 2,3,5-triphe-nylterazolium chloride and hematoxylin and eosin staining were used to determine brain damage in rats. cell viability was measured to evaluate the injury of OGd/R Pc12 cells. Western blotting was used to examine the expression of proteins associated with apoptosis and caSR. The caSR antagonist NPS-2143 and agonist Gdcl 3 were used to further confirm the effects of caSR during the process of apoptosis. The results demonstrated that Astragaloside IV alleviated cIRI by decreasing the NFS of rats, reducing the infarction volume of the brain and promoting the viability of Pc12 cells, as well as inhibiting the expression of cleaved caspase-3 and caSR, which was induced by cIRI. The results of the present study suggested that the activation of caSR may be involved in cIRI-induced brain damage in rats, and that Astragaloside IV may alleviate cIRI by inhibiting caSR activation-induced apoptosis.

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Effect of Acupuncture on Oxidative Stress Induced by Cerebral Ischemia-Reperfusion Injury

Cited by 33 publications

References 58 publications

miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

The effect of scalp electroacupuncture combined with Memantine in patients with vascular dementia

Astragaloside IV attenuates cerebral ischemia‑reperfusion injury in rats through the inhibition of calcium‑sensing receptor‑mediated apoptosis

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