Neuroprotective Effects of (−)-Epigallocatechin-3-Gallate Against Focal Cerebral Ischemia/Reperfusion Injury in Rats Through Attenuation of Inflammation

Zhang, Fengjin; Li, Na; Lin-lan, Jiang; Chen, LongHao; Huang, MuTu

doi:10.1007/s11064-015-1647-5

Cited by 45 publications

(22 citation statements)

References 45 publications

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“…In the present study, the level of NO, and the activities of TNOS, iNOS and cNOS were detected 24 h following the induction of cerebral ischemia. The levels of NO, TNOS, iNOS and cNOS significantly increased in the MCAO model group, which is consistent with the results of previous studies ( 8 – 10 ). The levels of NO, TNOS, iNOS and cNOS significantly decreased in the two IPTF pretreatment groups when compared to the model group.…”

Section: Discussionsupporting

confidence: 92%

“…These high levels lead to marked local and systemic inflammatory responses ( 8 , 9 ). Inflammation itself may exacerbate the spread of damage to the ischemic penumbra, increase the levels of inflammatory cytokines and thus, further aggravate brain injury ( 10 ). Therefore, the identification of novel drugs to regulate the inflammatory response is a promising method for the treatment of cerebral ischemic injury.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effect of total flavonoids from Ilex pubescens against focal cerebral ischemia/reperfusion injury in rats

Fang

Qiao

et al. 2017

Molecular Medicine Reports

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Ilex pubescens is commonly used in traditional Chinese medicine to treat cardiovascular and cerebrovascular diseases, such as coronary artery disease and stroke. However, the underlying mechanisms remain to be fully elucidated. The aim of the present study was to investigate the effects of Ilex pubescens total flavonoids (IPTF) on neuroprotection and the potential mechanisms in a rat model of focal cerebral ischemia/reperfusion (I/R) injury. Rats were pretreated with intragastric administration of IPTF at doses of 200 and 100 mg/kg for 5 days; middle cerebral artery occlusion surgery was then performed to induce cerebral I/R injury. Neurological deficits were determined using the 5-point neurological function score evaluation system, brain infarct sizes were determined by 2,3,5-triphenyltetrazolium chloride staining and alterations in brain histology were determined by hematoxylin and eosin staining. The neurological deficit score, the infarcted area and the brain tissue pathological injury were significantly reduced when the rats were pretreated with IPTF. In addition, inflammatory mediators and neurotrophic factors in the brain were investigated. IPTF pretreatment decreased the activities of total nitric oxide synthase (TNOS), induced NOS (iNOS) and constitutive NOS (cNOS), and the levels of nitric oxide (NO), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), however, it increased the levels of IL-10 in brain tissues. Furthermore, pretreatment with IPTF also increased the protein expressions of brain-derived neurotrophic factor, glial cell-derived neurotrophic factor and vascular endothelial growth factor, when compared with the model group. In conclusion, the results of the present study demonstrated that IPTF has a neuroprotective effect against focal cerebral I/R injury in rats. The mechanism may be associated with the decreased production of certain proinflammatory cytokines including NO, IL-1β, TNF-α, TNOS, iNOS and cNOS, the increased production of the anti-inflammatory cytokine IL-10 and the increased secretion of neurotrophic factors.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of total flavonoids from Ilex pubescens against focal cerebral ischemia/reperfusion injury in rats

Fang

Qiao

et al. 2017

Molecular Medicine Reports

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“…12-14 EGCG has also been shown to suppress interferon gamma-induced phosphorylation of STAT1 at its Ser 727 and Tyr 701 residues in cancer cells and to suppress cisplatin-induced phosphorylation selectively Ser 727 in response to cisplatin in the cochlea. 4 In aspiration-induced lung tissue injury, pre-treatment with EGCG reduced levels of cytokines (TNFα and IL-1), of activated STAT1 protein, and of phosphorylated protein levels of JAK1 and JAK2, 15 which may be attributed to blockade of INF-γ induced STAT1 activation.…”

Section: Discussionmentioning

confidence: 99%

Role of STAT1 and Oxidative Stress in Gentamicin-Induced Hair Cell Death in Organ of Corti

Jiang

Ray

Rybak³

et al. 2016

Otology &Amp; Neurotology

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Rationale Oxidative stress plays a critical role in gentamicin-induced hair cell death. Prior work has implicated the cytoplasmic transcription factor STAT1 as a potential mediator of drug-induced ototoxicity, but role in aminoglycosides is largely unknown. This study investigated aminoglycosides-induced cell death, exploring contributions of reactive oxygen species and STAT1 pathway in injury and protection. Methods Neonatal murine organ of Corti explants from 2-3 day postnatal pups (n=96) were treated with gentamicin at (4 μΜ, 50 μΜ) for 4-72 hours, with/without protectants. Effects on STAT1 pathway and gentamicin-induced hair cell death were measured with 50 μΜ Epigallocatechin Gallate (EGCG, a STAT1 inhibitor) and all-trans retinoic acid (atRA, a STAT1 activator). Hair cell morphology was evaluated and hair cell loss was quantified with cytocochleograms. Mitochondrial membrane potential was assayed and superoxide generation and suppression was measured with dihydroethidium (DHE) staining. Results Co-administration of 50 μΜ EGCG conferred protection from 4 μΜ gentamicin toxicity (p < 0.001), whereas atRA potentiated gentamicin-induced hair cell death (p<.001). On immunohistochemistry, STAT1 phosphorylation at theserine 727 (Ser727) residues was increased at 72 hours with 4 μΜ gentamicin. With administration of 50 μΜ gentamicin, there was activation of STAT1 Tyr701 at 4 hours and STAT1 Ser727 at 16 hours. Gentamicin dissipated mitochondrial membrane potentials, and EGCG attenuated gentamicin-induced oxidative stress at 72 hours. Conclusion EGCG protected outer hair cells from gentamicin toxicity in a cochlear explant model, with the underlying mechanism involving both reactive oxygen species (ROS) suppression and STAT1 inhibition.

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“…Stroke is the second cause of death and the leading cause of adult neurological disability worldwide 1 – 3 . Cerebral ischemic stroke accounts for 87% of all stroke cases.…”

Section: Introductionmentioning

confidence: 99%

Intravenous infusion of human bone marrow mesenchymal stromal cells promotes functional recovery and neuroplasticity after ischemic stroke in mice

Sammali

Alia

Vegliante

et al. 2017

Sci Rep

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Transplantation of human bone marrow mesenchymal stromal cells (hBM-MSC) promotes functional recovery after stroke in animal models, but the mechanisms underlying these effects remain incompletely understood. We tested the efficacy of Good Manufacturing Practices (GMP) compliant hBM-MSC, injected intravenously 3.5 hours after injury in mice subjected to transient middle cerebral artery occlusion (tMCAo). We addressed whether hBM-MSC are efficacious and if this efficacy is associated with cortical circuit reorganization using neuroanatomical analysis of GABAergic neurons (parvalbumin; PV-positive cells) and perineuronal nets (PNN), a specialized extracellular matrix structure which acts as an inhibitor of neural plasticity. tMCAo mice receiving hBM-MSC, showed early and lasting improvement of sensorimotor and cognitive functions compared to control tMCAo mice. Furthermore, 5 weeks post-tMCAo, hBM-MSC induced a significant rescue of ipsilateral cortical neurons; an increased proportion of PV-positive neurons in the perilesional cortex, suggesting GABAergic interneurons preservation; and a lower percentage of PV-positive cells surrounded by PNN, indicating an enhanced plastic potential of the perilesional cortex. These results show that hBM-MSC improve functional recovery and stimulate neuroprotection after stroke. Moreover, the downregulation of “plasticity brakes” such as PNN suggests that hBM-MSC treatment stimulates plasticity and formation of new connections in the perilesional cortex.

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Neuroprotective Effects of (−)-Epigallocatechin-3-Gallate Against Focal Cerebral Ischemia/Reperfusion Injury in Rats Through Attenuation of Inflammation

Cited by 45 publications

References 45 publications

Neuroprotective effect of total flavonoids from Ilex pubescens against focal cerebral ischemia/reperfusion injury in rats

Neuroprotective effect of total flavonoids from Ilex pubescens against focal cerebral ischemia/reperfusion injury in rats

Role of STAT1 and Oxidative Stress in Gentamicin-Induced Hair Cell Death in Organ of Corti

Intravenous infusion of human bone marrow mesenchymal stromal cells promotes functional recovery and neuroplasticity after ischemic stroke in mice

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