Transcriptional Regulation of Antioxidant Enzymes Activity and Modulation of Oxidative Stress by Melatonin in Rats Under Cerebral Ischemia / Reperfusion Conditions

Крыльский, Е. Д.; Popova, T. N.; Сафонова, О. А.; Stolyarova, A O; Razuvaev, G. A.; Carvalho, Miguel Angelo Pinheiro de

doi:10.1016/j.neuroscience.2019.01.046

Cited by 37 publications

(24 citation statements)

References 57 publications

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“…The enzymatic systems include superoxide dismutase (SOD), thioredoxin (Trx), paraoxonase (PON), glutathione peroxidase (GSHPx), catalase (CAT), glutathione s-transferase (GST), and others. Non-enzymatic systems include glutathione (GSH), vitamin A, vitamin C, Vitamin E, and carotenoids (Kryl'skii et al, 2019). Studies have confirmed that T-AOC regulation can protect neuronal damage in CIRI (Deng et al, 2015;Lin et al, 2015;Kryl'skii et al, 2019).…”

Section: Enzymatic and Non-enzymatic Antioxidant Systemsmentioning

confidence: 99%

“…Non-enzymatic systems include glutathione (GSH), vitamin A, vitamin C, Vitamin E, and carotenoids (Kryl'skii et al, 2019). Studies have confirmed that T-AOC regulation can protect neuronal damage in CIRI (Deng et al, 2015;Lin et al, 2015;Kryl'skii et al, 2019). α-lipoic acid exerted its neuroprotective effects through reversing the levels of oxidative parameters, including malondialdehyde (MDA), nitric oxide (NO), T-AOC, and SOD to their normal state in rat brains following CIRI (Deng et al, 2015).…”

Section: Enzymatic and Non-enzymatic Antioxidant Systemsmentioning

confidence: 99%

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Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

300

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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Section: Enzymatic and Non-enzymatic Antioxidant Systemsmentioning

confidence: 99%

Section: Enzymatic and Non-enzymatic Antioxidant Systemsmentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

300

197

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“…Taken together, pretreated 30 mg/kg CGA can provide a neuroprotective effect via upregulation of antioxidant enzymes which scavenge overproduced ROS in the CA1 pyramidal neurons following TFI. This is supported by a number of studies that have demonstrated that increased antioxidant enzymes create neuronal resistibility against ischemia-reperfusion injury by attenuating oxidative stress [ 11 , 30 , 35 , 43 , 44 ].…”

Section: Discussionmentioning

confidence: 90%

Experimental Pretreatment with Chlorogenic Acid Prevents Transient Ischemia-Induced Cognitive Decline and Neuronal Damage in the Hippocampus through Anti-Oxidative and Anti-Inflammatory Effects

et al. 2020

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Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is among the phenolic acid compounds which can be naturally found in green coffee extract and tea. CGA has been studied since it displays significant pharmacological properties. The aim of this study was to investigate the effects of CGA on cognitive function and neuroprotection including its mechanisms in the hippocampus following transient forebrain ischemia in gerbils. Memory and learning following the ischemia was investigated by eight-arm radial maze and passive avoidance tests. Neuroprotection was examined by immunohistochemistry for neuronal nuclei-specific protein and Fluoro-Jade B histofluorescence staining. For mechanisms of the neuroprotection, alterations in copper, zinc-superoxide dismutase (SOD1), SOD2 as antioxidant enzymes, dihydroethidium and 4-hydroxy-2-nonenal as indicators for oxidative stress, and anti-inflammatory cytokines (interleukin (IL)-4 and IL-13) and pro-inflammatory cytokines (tumor necrosis factor α (TNF-α) and IL-2) were examined by Western blotting and/or immunohistochemistry. As a result, pretreatment with 30 mg/kg CGA attenuated cognitive impairment and displayed a neuroprotective effect against transient forebrain ischemia (TFI). In Western blotting, the expression levels of SOD2 and IL-4 were increased due to pretreatment with CGA and, furthermore, 4-HNE production and IL-4 expressions were inhibited by CGA pretreatment. Additionally, pretreated CGA enhanced antioxidant enzymes and anti-inflammatory cytokines and, in contrast, attenuated oxidative stress and pro-inflammatory cytokine expression. Based on these results, we suggest that CGA can be a useful neuroprotective material against ischemia-reperfusion injury due to its antioxidant and anti-inflammatory efficacies.

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“…However, some murine model studies have shown that after the oral administration of tea, different substances of tea are brain permeable and have neuroprotective effects (by increasing antioxidant capacity in brain samples) (Pervin et al, 2019;Rashid et al, 2014). Oxidative stress and antioxidant capacity in brain samples have been reduced in cerebral ischemia animal models with melatonin administration (Blanco et al, 2017;Kryl'skii et al, 2019). Also, oxidative stress measured in plasma has been reduced by different antioxidant vitamins administered orally in patients with acute ischemic stroke (E, C, B2, B6, B12) (Ullegaddi et al, 2004(Ullegaddi et al, , 2005(Ullegaddi et al, , 2006.…”

Section: Discussionmentioning

confidence: 99%

Mortality prediction of ischemic stroke patients without thrombectomy by blood total antioxidant capacity

Lorente¹,

Martı́n²,

González-Rivero³

et al. 2020

Journal of Integrative Neuroscience

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Transcriptional Regulation of Antioxidant Enzymes Activity and Modulation of Oxidative Stress by Melatonin in Rats Under Cerebral Ischemia / Reperfusion Conditions

Cited by 37 publications

References 57 publications

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Experimental Pretreatment with Chlorogenic Acid Prevents Transient Ischemia-Induced Cognitive Decline and Neuronal Damage in the Hippocampus through Anti-Oxidative and Anti-Inflammatory Effects

Mortality prediction of ischemic stroke patients without thrombectomy by blood total antioxidant capacity

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