(−)-Epigallocatechin Gallate Protects Against Cerebral Ischemia-Induced Oxidative Stress via Nrf2/ARE Signaling

Han, Jie; Wang, Miaomiao; Xu, Jing; Shi, Hui; Ren, Manru; Lou, Haiyan

doi:10.1007/s11064-014-1311-5

Cited by 96 publications

(56 citation statements)

References 23 publications

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“…Compared with WT mice, Nrf2 −/− mice suffered more brain damage in a cerebral ischemia model [107, 108]. In recent preclinical studies, sulforaphane [109], ursolic acid [110], erythropoietin [111], and (−)-epigallocatechin gallate [112] were shown to protect against brain damage after ischemic stroke by activating the Nrf2 pathway. However, Nrf2 has not been as well studied in ICH as it has been in ischemic stroke.…”

Section: Microgliamentioning

confidence: 99%

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

et al. 2016

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Intracerebral hemorrhage (ICH) is a subtype of stroke with high mortality and morbidity. When a diseased artery within the brain bursts, expansion and absorption of the resulting hematoma trigger a series of reactions that cause primary and secondary brain injury. Microglia are extremely important for removing the hematoma and clearing debris, but they are also a source of ongoing inflammation. This article discusses the role of microglial activation/polarization and related inflammatory mediators, such as Toll-like receptor 4, matrix metalloproteinases, high-mobility group protein box-1, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron, in secondary injury after ICH and highlights the potential targets for ICH treatment.

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Section: Microgliamentioning

confidence: 99%

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

et al. 2016

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“…have reported protective effects of EGCG against ischemia/reperfusion injury in a rat model of MCAO (119). Administration of EGCG improved neurologic scores, reduced infarct volume, and ameliorated neuronal apoptosis due to increased GSH biosynthesis (via Nrf2 activation) and decreased ROS content.…”

Section: Phytochemicals With Nrf2-are Activating Abilitymentioning

confidence: 99%

Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases

Sun

Yang

Leak

et al. 2017

CNSNDDT

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Central nervous system diseases are major health issues and are often associated with disability or death. Most central nervous system disorders are characterized by high levels of oxidative stress. Nuclear factor erythroid 2 related factor (Nrf2) is known for its ability to regulate the expression of a series of enzymes with antioxidative, prosurvival, and detoxification effects. Under basal conditions, Nrf2 forms a complex with Kelch-like ECH associated protein 1, leading to Nrf2 inactivation via ubiquitination and degradation. However, following exposure of Keap1 to oxidative stress, Nrf2 is released from Keap1, activated, and translocated into the nucleus. Upon nuclear entry, Nrf2 binds to antioxidant response elements (ARE), thereby inducing the expression of genes such as glutathione s-transferase, heme oxygenase 1, and NADPH quinine oxidoreductase 1. Many dietary phytochemicals have been reported to activate the protective Nrf2/ARE pathway. Here, we review the preventive and protective effects of dietary Nrf2 activators against CNS diseases, including stroke, traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease.

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“…Nrf2 binds to the antioxidant response element (ARE) in the promoter region of several genes, and it is an upstream regulator of the encoding of antioxidative proteins, such as heme oxygenase 1 (HO-1), which antagonize reactive oxygen species (ROS)-induced oxidative stress [7,8].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

Zhou

Che

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ischemia-reperfusion (I/R) adversely affects the intestinal mucosa. The major mechanisms of I/R are the generation of reactive oxygen species (ROS) and apoptosis. Salvianolic acid A (SalA) is suggested to be an effective antioxidative and antiapoptotic agent in numerous pathological injuries. The present study investigated the protective role of SalA in I/R of the intestine. Methods: Adult male Sprague-Dawley rats were subjected to intestinal I/R injury in vivo. In vitro experiments were performed in IEC-6 cells subjected to hypoxia/ reoxygenation (H/R) stimulation to simulate intestinal I/R. TNF-α, IL-1β, and IL-6 levels were measured using enzyme-linked immunosorbent assay. Malondialdehyde and myeloperoxidase and glutathione peroxidase levels were measured using biochemical analysis. Apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling staining or flow cytometry in vivo and in vitro. The level of reactive oxygen species (ROS) was measured by dichlorodihydrofluorescin diacetate (DCFH-DA) staining. Western blotting was performed to determine the expression of heme oxygenase-1 (HO-1), Nrf2 and proteins associated with apoptosis. The mRNA expressions of Nrf2 and HO-1 were detected by quantitative real-time polymerase chain reaction in vivo and in vitro. Results: Malondialdehyde level and myeloperoxidase and glutathione peroxidase, TNF-α, IL-1β, and IL-6 levels group in intestinal tissue decreased significantly in the SalA pretreatment groups compared to the I/R group. SalA markedly abolished intestinal injury compared to the I/R group. SalA significantly attenuated apoptosis and increased Nrf2/HO-1 expression in vivo and in vitro. However, Nrf2 siRNA treatment partially abrogated the above mentioned effects of SalA in H/R-induced ROS and apoptosis in IEC-6 cells. Conclusion: The present study demonstrated that SalA ameliorated oxidation, inhibited the release of pro-inflammatory cytokines and alleviated apoptosis in I/R-induced injury and that these protective effects may partially occur via regulation of the Nrf2/ HO-1 pathways.

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(−)-Epigallocatechin Gallate Protects Against Cerebral Ischemia-Induced Oxidative Stress via Nrf2/ARE Signaling

Cited by 96 publications

References 23 publications

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

Microglial Polarization and Inflammatory Mediators After Intracerebral Hemorrhage

Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases

Salvianolic Acid A Protects Against Oxidative Stress and Apoptosis Induced by Intestinal Ischemia-Reperfusion Injury Through Activation of Nrf2/HO-1 Pathways

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