Ginsenoside compound K protects against cerebral ischemia/reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

Huang, Qingxia; Li, Jing; Chen, Jinjin; Zhang, Zepeng; Xu, Peng; Qi, Hongyu; Chen, Zhaoqiang; Liu, Jiaqi; Lü, Jing; Shi, M.; Zhang, Yibin; Ma, Ying; Zhao, Daqing; Li, Xiangyan

doi:10.1016/j.jgr.2022.10.004

Cited by 7 publications

(5 citation statements)

References 40 publications

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“…However, its potential role in preventing cerebral stroke ischemia-reperfusion injury remains unclear. Huang QX et al ( Huang et al, 2023 ) confirmed through in vitro and in vivo models that GCK pretreatment could alleviate Drp1 mitochondrial translocation, mitochondrial autophagy, mitochondrial apoptosis, and neuronal bioenergetic imbalance, thus inhibiting stroke ischemia-reperfusion injury. Furthermore, GCK treatment could decrease the binding affinity of Mul1 and Mfn2, inhibit Mul1/Mfn2-mediated ubiquitination and degradation, and increase the protein level of Mfn2 in cerebral ischemia-reperfusion injury.…”

Section: Medicinal Plants and Their Active Metabolites Alleviate Cere...mentioning

confidence: 99%

Progress of medicinal plants and their active metabolites in ischemia-reperfusion injury of stroke: a novel therapeutic strategy based on regulation of crosstalk between mitophagy and ferroptosis

Zhang,

Wang,

Jiang

et al. 2024

Front. Pharmacol.

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The death of cells can occur through various pathways, including apoptosis, necroptosis, mitophagy, pyroptosis, endoplasmic reticulum stress, oxidative stress, ferroptosis, cuproptosis, and disulfide-driven necrosis. Increasing evidence suggests that mitophagy and ferroptosis play crucial regulatory roles in the development of stroke. In recent years, the incidence of stroke has been gradually increasing, posing a significant threat to human health. Hemorrhagic stroke accounts for only 15% of all strokes, while ischemic stroke is the predominant type, representing 85% of all stroke cases. Ischemic stroke refers to a clinical syndrome characterized by local ischemic-hypoxic necrosis of brain tissue due to various cerebrovascular disorders, leading to rapid onset of corresponding neurological deficits. Currently, specific therapeutic approaches targeting the pathophysiological mechanisms of ischemic brain tissue injury mainly include intravenous thrombolysis and endovascular intervention. Despite some clinical efficacy, these approaches inevitably lead to ischemia-reperfusion injury. Therefore, exploration of treatment options for ischemic stroke remains a challenging task. In light of this background, advancements in targeted therapy for cerebrovascular diseases through mitophagy and ferroptosis offer a new direction for the treatment of such diseases. In this review, we summarize the progress of mitophagy and ferroptosis in regulating ischemia-reperfusion injury in stroke and emphasize their potential molecular mechanisms in the pathogenesis. Importantly, we systematically elucidate the role of medicinal plants and their active metabolites in targeting mitophagy and ferroptosis in ischemia-reperfusion injury in stroke, providing new insights and perspectives for the clinical development of therapeutic drugs for these diseases.

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Section: Medicinal Plants and Their Active Metabolites Alleviate Cere...mentioning

confidence: 99%

Progress of medicinal plants and their active metabolites in ischemia-reperfusion injury of stroke: a novel therapeutic strategy based on regulation of crosstalk between mitophagy and ferroptosis

Zhang,

Wang,

Jiang

et al. 2024

Front. Pharmacol.

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“…Panax ginseng is a Chinese herbal medicine that has been used as a tonic medicine for centuries in China. Ginsenoside compound K(CK) , an important saponin-like component of ginseng, augmented mitochondrial fusion and attenuated mitophagy in cerebral IR injury through the Mul1/Mfn2 pathway ( Huang et al, 2023b ). The study found that Ginsenoside CK inhibited mitochondrial dynamics imbalance and damage by reducing the binding affinity of Mul1 and Mfn2, which in turn inhibited the ubiquitination of Mfn2 by Mul1.…”

Section: Regulation For Management Of Cerebral I/r Injurymentioning

confidence: 99%

“…Ginsenoside CK reduced mitochondrial fission and mitophagy, counteracting I/R-induced neurological impairment and mitochondrial dysfunction. The mitigation effect of ginsenoside CK on mitophagy was markedly abrogated by Mfn2 knockdown ( Huang et al, 2023b ).…”

Section: Regulation For Management Of Cerebral I/r Injurymentioning

confidence: 99%

“…Animal and cellular experiments have further demonstrated that CHM monomers and decoctions can improve ischemic stroke symptoms and provide neuroprotection by attenuating cerebral I/R injury ( Ding et al, 2019 ; Jiao-Yan et al, 2021 ; Tang et al, 2021 ; Ni et al, 2022 ; Liao et al, 2023 ). These studies have found that many Chinese medicines, including monomers and decoctions, can attenuate cerebral I/R injury by modulating mitophagy ( Zhang et al, 2020a ; Han et al, 2022a ; Ji et al, 2022a ; Huang et al, 2023a ). Interestingly, some of these medicines work by inhibiting mitophagy, while others work by activating it.…”

Section: Introductionmentioning

confidence: 99%

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The neuroprotective effect of Chinese herbal medicine for cerebral ischemia reperfusion injury through regulating mitophagy

Chen,

Zhang,

et al. 2024

Front. Pharmacol.

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The incidence of ischemic stroke has been increasing annually with an unfavorable prognosis. Cerebral ischemia reperfusion injury can exacerbate nerve damage. Effective mitochondrial quality control including mitochondrial fission, fusion and autophagy, is crucial for maintaining cellular homeostasis. Several studies have revealed the critical role of mitophagy in Cerebral ischemia reperfusion injury. Cerebral ischemia and hypoxia induce mitophagy, and mitophagy exhibits positive and negative effects in cerebral ischemia reperfusion injury. Studies have shown that Chinese herbal medicine can alleviate Cerebral ischemia reperfusion injury and serve as a neuroprotective agent by inhibiting or promoting mitophagy-mediated pathways. This review focuses on the mitochondrial dynamics and mitophagy-related pathways, as well as the role of mitophagy in ischemia reperfusion injury. Additionally, it discusses the therapeutic potential and benefits of Chinese herbal monomers and decoctions in the treatment of ischemic stroke.

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“…Additionally, the effect of YC-1101 was also compared with several compounds known to restore mitochondria, such as red ginseng [21], AGCP [22], aloe gel [23], beta-glucan [24], and compound K [25]. Initially, the appropriate concentration of each compound was determined using the MTT assay.…”

Section: Cellular Toxicity Of Yc-1101 and Other Compounds In Primary ...mentioning

confidence: 99%

Protective effects of enzymatically digested velvet antler polypeptides on mitochondria in primary astrocytes

Paing,

Lee

2023

J Anim Sci Technol

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ORCID (for more information, please visit https://orcid.org) Yunn Me Me Paing (https://orcid.org/0000-0003-4116-9534) Sung Hoon Lee (https://orcid.org/0000-0002-1805-8281) Competing interestsNo potential conflict of interest relevant to this article was reported. Funding sourcesState funding sources (grants, funding sources, equipment, and supplies). Include name and number of grant if available.Not applicable.

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Ginsenoside compound K protects against cerebral ischemia/reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

Cited by 7 publications

References 40 publications

Progress of medicinal plants and their active metabolites in ischemia-reperfusion injury of stroke: a novel therapeutic strategy based on regulation of crosstalk between mitophagy and ferroptosis

Progress of medicinal plants and their active metabolites in ischemia-reperfusion injury of stroke: a novel therapeutic strategy based on regulation of crosstalk between mitophagy and ferroptosis

The neuroprotective effect of Chinese herbal medicine for cerebral ischemia reperfusion injury through regulating mitophagy

Protective effects of enzymatically digested velvet antler polypeptides on mitochondria in primary astrocytes

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