Epigallocatechin-3-Gallate Reduces Neuronal Apoptosis in Rats after Middle Cerebral Artery Occlusion Injury via PI3K/AKT/eNOS Signaling Pathway

Wang, Nan; Xu, Zhijun; Chen, Keyan; Liu, Tongtong; Guo, Wanshu; Zhou, Xu

doi:10.1155/2018/6473580

Cited by 50 publications

(40 citation statements)

References 27 publications

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“…PI3K/Akt is a transmembrane signal transduction cascade involved in the growth and apoptosis of myocardial cells, which also regulate coronary angiogenesis and downstream signal transduction . He et al demonstrated that activating the PI3K/Akt/eNOS signaling pathway attenuates myocardial apoptosis induced by ischemic‐reperfusion (I/R) in mice via cleaving caspase‐3 expression, elevating the Bcl‐2/Bax ratio, and restoring NO production.…”

Section: Introductionmentioning

confidence: 99%

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Liu

et al. 2018

Cardiovascular Therapeutics

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Summary Introduction Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary. Aim In order to explore the protective effect of hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN‐T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphine. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down‐regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.

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Section: Introductionmentioning

confidence: 99%

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Liu

et al. 2018

Cardiovascular Therapeutics

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“…It follows the mTOR-AMPK pathway in stressed ER and impaired the oxidative stress responses and enhance autophagy-dependent survival. It also promotes cell multiplication, differentiation, neovascularization, tube formation, and cell homing by associating the vascular endothelial growth factor (VEGF), regulation of BAX, Bcl-2, LC3B, caspase-3, mTOR and Beclin-1 [187]. It has also protected HBMVECs from Ischemia/Reperfusion injury by ameliorating apoptosis and autophagy and promoting neurovascularization [105].…”

Section: Vascular Cognitive Impairmentmentioning

confidence: 99%

Neuroprotection: Targeting Multiple Pathways by Naturally Occurring Phytochemicals

et al. 2020

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With the increase in the expectancy of the life span of humans, neurodegenerative diseases (NDs) have imposed a considerable burden on the family, society, and nation. In defiance of the breakthroughs in the knowledge of the pathogenesis and underlying mechanisms of various NDs, very little success has been achieved in developing effective therapies. This review draws a bead on the availability of the nutraceuticals to date for various NDs (Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, Huntington’s disease, vascular cognitive impairment, Prion disease, Spinocerebellar ataxia, Spinal muscular atrophy, Frontotemporal dementia, and Pick’s disease) focusing on their various mechanisms of action in various in vivo and in vitro models of NDs. This review is distinctive in its compilation to critically review preclinical and clinical studies of the maximum phytochemicals in amelioration and prevention of almost all kinds of neurodegenerative diseases and address their possible mechanism of action. PubMed, Embase, and Cochrane Library searches were used for preclinical studies, while ClinicalTrials.gov and PubMed were searched for clinical updates. The results from preclinical studies demonstrate the efficacious effects of the phytochemicals in various NDs while clinical reports showing mixed results with promise for phytochemical use as an adjunct to the conventional treatment in various NDs. These studies together suggest that phytochemicals can significantly act upon different mechanisms of disease such as oxidative stress, inflammation, apoptotic pathways, and gene regulation. However, further clinical studies are needed that should include the appropriate biomarkers of NDs and the effect of phytochemicals on them as well as targeting the appropriate population.

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“…In addition, EGCG (2.5 mg/kg for 2 weeks) in the dentate gyrus has been shown to promote the proliferation of neuronal precursor cells as well as inhibit apoptosis in the hippocampus [ 72 ]. Moreover, EGCG (administered intraperitoneally, at a dose of 20 mg/kg) in rat models with I/R injury reduced neurological deficits, decreased oxidative stress and levels of brain injury markers, promoted neuron survival, and inhibited the apoptosis of neuronal cells through the upregulation of Bcl-2 expression and the downregulation of Bax and Caspase-3 [ 66 ].…”

Section: Flavonoidsmentioning

confidence: 99%

Flavonoids as a Natural Enhancer of Neuroplasticity—An Overview of the Mechanism of Neurorestorative Action

et al. 2020

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Neuroplasticity is a complex physiological process occurring in the brain for its entire life. However, it is of particular importance in the case of central nervous system (CNS) disorders. Neurological recovery largely depends on the ability to reestablish the structural and functional organization of neurovascular networks, which must be pharmacologically supported. For this reason, new forms of therapy are constantly being sought. Including adjuvant therapies in standard treatment may support the enhancement of repair processes and restore impaired brain functions. The common hallmark of nerve tissue damage is increased by oxidative stress and inflammation. Thus, the studies on flavonoids with strong antioxidant and anti-inflammatory properties as a potential application in neuro intervention have been carried out for a long time. However, recent results have revealed another important property of these compounds in CNS therapy. Flavonoids possess neuroprotective activity, and promote synaptogenesis and neurogenesis, by, among other means, inhibiting oxidative stress and neuroinflammation. This paper presents an overview of the latest knowledge on the impact of flavonoids on the plasticity processes of the brain, taking into account the molecular basis of their activity.

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Epigallocatechin-3-Gallate Reduces Neuronal Apoptosis in Rats after Middle Cerebral Artery Occlusion Injury via PI3K/AKT/eNOS Signaling Pathway

Cited by 50 publications

References 27 publications

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Neuroprotection: Targeting Multiple Pathways by Naturally Occurring Phytochemicals

Flavonoids as a Natural Enhancer of Neuroplasticity—An Overview of the Mechanism of Neurorestorative Action

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