Compound K inhibits autophagy-mediated apoptosis induced by oxygen and glucose deprivation/reperfusion via regulating AMPK-mTOR pathway in neurons

Huang, Qingxia; Lou, Tingting; Wang, Man-Ying; Xue, Linyuan; Lü, Jing; Zhang, He; Zhang, Zepeng; Wang, Hui; Jing, Chuanyong; Zhao, Daqing; Sun, Liwei; Li, Xiangyan

doi:10.1016/j.lfs.2020.117793

Cited by 38 publications

(22 citation statements)

References 42 publications

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“…Since apoptosis and autophagy are two death mechanisms that mediate cell fate, emphasis has been placed upon linking the complex regulation between the two [ 49 ]. Compound K preconditioning decreased apoptosis after oxygen and glucose deprivation/reperfusion via inhibiting accelerated autophagy [ 20 ]. There have also been reported links combining autophagy and apoptosis through interactions of specific proteins between the two processes [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

“…Autophagy is a self-degrading process that maintains homeostasis by removing superfluous organelles and damaged proteins through a lysosome pathway [16,17]. Both in vitro and in vivo experiments provide evidence that autophagy is activated after ischemia [18][19][20][21]. It is reported that hyperbaric oxygen (HBO) regulates ischemia-induced autophagy and apoptosis and produces a neuroprotective effect by promoting the recovery of neural function [22].…”

Section: Introductionmentioning

confidence: 99%

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Normobaric Oxygen (NBO) Therapy Reduces Cerebral Ischemia/Reperfusion Injury through Inhibition of Early Autophagy

Wang

Dandu

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Objectives. Normobaric oxygen (NBO) therapy has great clinical potential in the treatment of ischemic stroke, but its underlying mechanism is unknown. Our study aimed to investigate the role of autophagy during the application of NBO on cerebral ischemia/reperfusion injury. Methods. Male Sprague Dawley rats received 2 hours of middle cerebral artery occlusion (MCAO), followed by 2, 6, or 24 hours of reperfusion. At the beginning of reperfusion, rats were randomly given NBO (95% O2) or room air (21% O2) for 2 hours. In some animals, 3-methyladenine (3-MA, autophagy inhibitor) was administered 10 minutes before reperfusion. The severity of the ischemic injury was determined by infarct volume, neurological deficit, and apoptotic cell death. Western blotting was used to determine the protein expression of autophagy and apoptosis, while mRNA expression of apoptotic molecules was detected by real-time PCR. Results. NBO treatment after ischemia/reperfusion significantly decreased infarct volume and neurobehavioral defects. The increased expression of the autophagy markers, including microtubule-associated protein 1A light chain 3 (LC3) and Beclin 1, after ischemia/reperfusion was reversed by NBO, while promoting Sequestosome 1 (p62/SQSTM1) expression. In addition, NBO reduced cerebral apoptosis in association with alleviated BAX expression and increased BCL-2 expression. 3-MA reduced autophagy and apoptotic death but did not further improve NBO-attenuated ischemic damage. Conclusion. NBO induced remarkable neuroprotection from ischemic injury, which was correlated with blocked autophagy activity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Normobaric Oxygen (NBO) Therapy Reduces Cerebral Ischemia/Reperfusion Injury through Inhibition of Early Autophagy

Wang

Dandu

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…A previous report showed that Sodium tanshinone IIA sulfonate treatment reduced neuroinflammation and reduced the up‐regulation of autophagy associated proteins, 88 and a report has shown that pretreatment with Compound K (CK) prevented neurons from OGD/R injury via decreasing the ROS generation and increasing cell capability, Ca 2+ overload and mitochondrial damage. Additionally, CK reduces autophagy‐mediated apoptosis via boosting the process of forming autophagosomes into phagocytic precursors 89 . A research implied that geniposide substantially diminished inflammatory response in BV‐2 microglial cells after OGD/R.…”

Section: Pharmacology Targeting Mqc In Strokementioning

confidence: 99%

Mitochondrial quality control in stroke: From the mechanisms to therapeutic potentials

Tian

Chen

Liao

et al. 2022

J Cellular Molecular Medi

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Mitochondrial damage is a critical contributor to stroke‐induced injury, and mitochondrial quality control (MQC) is the cornerstone of restoring mitochondrial homeostasis and plays an indispensable role in alleviating pathological process of stroke. Mitochondria quality control promotes neuronal survival via various adaptive responses for preserving mitochondria structure, morphology, quantity and function. The processes of mitochondrial fission and fusion allow for damaged mitochondria to be segregated and facilitate the equilibration of mitochondrial components such as DNA, proteins and metabolites. The process of mitophagy is responsible for the degradation and recycling of damaged mitochondria. This review aims to offer a synopsis of the molecular mechanisms involved in MQC for recapitulating our current understanding of the complex role that MQC plays in the progression of stroke. Speculating on the prospect that targeted manipulation of MQC mechanisms may be exploited for the rationale design of novel therapeutic interventions in the ischaemic stroke and haemorrhagic stroke. In the review, we highlight the potential of MQC as therapeutic targets for stroke treatment and provide valuable insights for clinical strategies.

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“…Protective autophagy is induced by the AMPK/mTOR/ UNC-51-like kinase-1 (ULK1) pathway in the CNS, facilitating the proliferation and migration of astrocytes after oxygen-glucose deprivation (OGD), and improves cerebral ischemia reperfusion injury to exert a neuroprotective effect (Zhang and Miao, 2018). Instead, a study conducted by Huang et al (2020) found that pretreatment with Ginsenoside monomer compound K, which can protect brain OGD and reperfusion (OGD/R) injury, markedly reduced p-AMPK level and increased the p-mTOR level, leading to neuroprotection against OGD/R-induced neural autophagy. Puerarin has been used for the treatment of cardio-cerebrovascular.…”

Section: The Mechanism Of Hypoxia-mediated Autophagy Of Immune Cells In the Cnsmentioning

confidence: 99%

The Role of Autophagy in Hypoxia-Induced Neuroinflammation

Sha

Tan

Miao

et al. 2021

DNA and Cell Biology

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Autophagy is a critical cytoprotective mechanism that takes a hand in innate or adaptive immune responses. Hypoxia is a common pathophysiological mechanism that can lead to systemic pathological reactions. In recent years, the impact of hypoxia on the central nervous system has attracted more attention. In the past, autophagy was thought to be directly involved in the apoptosis of nerve cells under hypoxia. An increasing amount of evidence shows that the neuroinflammatory response plays an indispensable role in the neural damage caused by hypoxia. There are many mechanisms related to the neuroinflammatory response induced by hypoxia, among which autophagy is an important aspect, but the role of autophagy is still unclear. This article focuses on how autophagy flux of central immune cells is modified under hypoxic conditions, and how this autophagy affects neuroinflammatory response.

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Compound K inhibits autophagy-mediated apoptosis induced by oxygen and glucose deprivation/reperfusion via regulating AMPK-mTOR pathway in neurons

Cited by 38 publications

References 42 publications

Normobaric Oxygen (NBO) Therapy Reduces Cerebral Ischemia/Reperfusion Injury through Inhibition of Early Autophagy

Normobaric Oxygen (NBO) Therapy Reduces Cerebral Ischemia/Reperfusion Injury through Inhibition of Early Autophagy

Mitochondrial quality control in stroke: From the mechanisms to therapeutic potentials

The Role of Autophagy in Hypoxia-Induced Neuroinflammation

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