Resveratrol attenuates hypoxia-induced neurotoxicity through inhibiting microglial activation

Zhang, Qun; Yuan, Lin; Zhang, Qingrui; Gao, Yan; Liu, Guangheng; Xia, Meng; Wei, Xiang; Wang, Zhen; Liu, Dexiang

doi:10.1016/j.intimp.2015.07.027

Cited by 38 publications

(35 citation statements)

References 41 publications

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“…Western blotting results indicate that the levels of NF-κB expression were not significantly changed in any group but that hypoxia slightly increased the phosphorylation of NF-κB (Fig. 4A, B), which is in agreement with previous observations (2). However, no significant changes in the phosphorylation of NF-κB were observed among the hypoxia-induced groups in the presence or absence of KHG26792 (Fig.…”

Section: Resultssupporting

confidence: 93%

“…BV-2 cells were pretreated with KHG26792 for 30 min followed by hypoxia for 24 h. The results of this assay demonstrated a 49% reduction in cell viability 24 h after hypoxia (Fig. 1A), which is in agreement with previous observations (2, 10). However, 50 μM KHG26792 rescued cells from hypoxia-induced toxicity to near normal viability levels (Fig.…”

Section: Resultssupporting

confidence: 92%

“…Hypoxia-induced microglial activation releases large quantities of NO through an increase in iNOS expression in response to brain damage (2). Herein we examined the effects of KHG26792 on the regulation of NO and iNOS levels in hypoxia-induced BV-2 cells.…”

Section: Resultsmentioning

confidence: 99%

“…For hypoxic exposure, cells were changed to hypoxia by placing them in a chamber with 3% oxygen, 5% CO 2 , and 92% nitrogen at 37°C. Cells serving as controls were incubated at 37°C with 95% air and 5% CO2 (2). For most experiments, BV-2 cells were pretreated with KHG26792 for 30 min followed by hypoxia for 24 h, while controls were treated with the vehicle except where indicated.…”

Section: Methodsmentioning

confidence: 99%

“…Microglial activation in the brain plays an important role in the progression of neurodegenerative pathologies; activated microglia secrete reactive oxygen species (ROS), chemokines, and pro-inflammatory cytokines that elicit neuroinflammatory responses and contribute to hypoxic brain injury (2). Because hypoxia can also promote neuronal injury through microglial activation during cerebral ischemia, inflammation may play an important role in the progression of both ischemic stroke and hypoxia (3), although the exact mechanism for microglial activation after ischemic injury remains unclear.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Protective effect of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on hypoxia-induced toxicity by suppressing microglial activation in BV-2 cells

Kim¹,

Kim²,

Na³

et al. 2016

BMB Reports

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We recently reported the anti-inflammatory effects of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride (KHG26792) on the ATP-induced activation of the NFAT and MAPK pathways through the P2X7 receptor in microglia. To further investigate the underlying mechanism of KHG26792, we studied its protective effects on hypoxia-induced toxicity in microglia. The administration of KHG26792 significantly reduced the hypoxia-induced expression and activity of caspase-3 in BV-2 microglial cells. KHG26792 also reduced hypoxia-induced inducible nitric oxide synthase protein expression, which correlated with reduced nitric oxide accumulation. In addition, KHG26792 attenuated hypoxia-induced protein nitration, reactive oxygen species production, and NADPH oxidase activity. These effects were accompanied by the suppression of hypoxia-induced protein expression of hypoxia-inducible factor 1-alpha and NADPH oxidase-2. Although the clinical relevance of our findings remains to be determined, these data results suggest that KHG26792 prevents hypoxia-induced toxicity by suppressing microglial activation.

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Section: Resultssupporting

confidence: 93%

Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Protective effect of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on hypoxia-induced toxicity by suppressing microglial activation in BV-2 cells

Kim¹,

Kim²,

Na³

et al. 2016

BMB Reports

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Resveratrol prevents cognitive deficits induced by sleep deprivation via modulating sirtuin 1 associated pathways in the hippocampus

Zhang,

Wei,

Zhang

et al. 2024

J Biochem & Molecular Tox

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Accumulating evidence confirms that sleep insufficiency is a high risk factor for cognitive impairment, which involves inflammation and synaptic dysfunction. Resveratrol, an agonist of the Sirt1, has demonstrated anti‐inflammation and neuroprotective effects in models of Alzheimer's disease, Parkinson's disease, and schizophrenia. However, the beneficial effects of resveratrol on sleep deprivation‐induced cognitive deficits and its underlying molecular mechanisms are unclear. In the present study, thirty‐two male C57BL/6 J mice were randomly divided into a Control+DMSO group, Control+Resveratrol group, SD+DMSO group, and SD+Resveratrol group. The mice in the SD+Resveratrol group underwent 5 days of sleep deprivation after pretreatment with resveratrol (50 mg/kg) for 2 weeks, while the mice in the SD+DMSO group only underwent sleep deprivation. After sleep deprivation, we evaluated spatial learning and memory function using the Morris water maze test. We used general molecular biology techniques to detect changes in levels of pro‐inflammatory cytokines and Sirt1/miR‐134 pathway‐related synaptic plasticity proteins. We found that resveratrol significantly reversed sleep deprivation‐induced learning and memory impairment, elevated interleukin‐1β, interleukin‐6, and tumor necrosis factor‐α levels, and decreased brain‐derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density protein‐95, and synaptophysin levels by activating the Sirt1/miR‐134 pathway. In conclusion, resveratrol is a promising agent for preventing sleep deprivation‐induced cognitive dysfunction by reducing pro‐inflammatory cytokines and improving synaptic function via the Sirt1/miR‐134 pathway.

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Aging, Immunity, and Neuroinflammation: The Modulatory Potential of Nutrition

Benedetto

Müller

2019

Nutrition and Immunity

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Resveratrol attenuates hypoxia-induced neurotoxicity through inhibiting microglial activation

Cited by 38 publications

References 41 publications

Protective effect of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on hypoxia-induced toxicity by suppressing microglial activation in BV-2 cells

Protective effect of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on hypoxia-induced toxicity by suppressing microglial activation in BV-2 cells

Resveratrol prevents cognitive deficits induced by sleep deprivation via modulating sirtuin 1 associated pathways in the hippocampus

Aging, Immunity, and Neuroinflammation: The Modulatory Potential of Nutrition

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