Ginkgolide B attenuates cerebral ischemia-reperfusion injury via inhibition of ferroptosis through disrupting NCOA4-FTH1 interaction

Yang, Yuwei; Wu, Qing; Shan, Xin; Zhou, Haïyan; Wang, J; Hu, Yahong; Chen, Jing; Lv, Zhiyang

doi:10.1016/j.jep.2023.116982

Cited by 11 publications

(7 citation statements)

References 43 publications

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“…In summary, the mechanisms underlying ferritinophagy and ferroptosis in CIRI require further research to identify effective therapeutic measures. Acupuncture therapy Electroacupuncture By decreasing ACSL4 and TfR1 expression and promoting GPX4 levels to inhibit ROS production and ferroptosis [110] Electroacupuncture pretreatment By modulating iron metabolism or increasing GSH/ GPX4 expression to reduce oxidative stress after CIRI [111] Moxibustion By reducing levels of lipid peroxides, malondialchehyche, ACSL4, hepcidin to inhibit ferroptosis [112] Ginkgolide B By disrupting NCOA4-FTH1 interaction to inhibit ferritinophagy and alleviate CIRI CIRI [125]…”

Section: Summary and Prospectmentioning

confidence: 99%

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

Liu,

Xie,

Wang

et al. 2024

Neurochem Res

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Cerebral ischemia–reperfusion injury (CIRI) is the second leading cause of death worldwide, posing a huge risk to human life and health. Therefore, investigating the pathogenesis underlying CIRI and developing effective treatments are essential. Ferroptosis is an iron-dependent mode of cell death, which is caused by disorders in iron metabolism and lipid peroxidation. Previous studies demonstrated that ferroptosis is also a form of autophagic cell death, and nuclear receptor coactivator 4(NCOA4) mediated ferritinophagy was found to regulate ferroptosis by interfering with iron metabolism. Ferritinophagy and ferroptosis are important pathogenic mechanisms in CIRI. This review mainly summarizes the link and regulation between ferritinophagy and ferroptosis and further discusses their mechanisms in CIRI. In addition, the potential treatment methods targeting ferritinophagy and ferroptosis for CIRI are presented, providing new ideas for the prevention and treatment of clinical CIRI in the future.

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Section: Summary and Prospectmentioning

confidence: 99%

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

Liu,

Xie,

Wang

et al. 2024

Neurochem Res

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“…Human neuromelanin isolated from substantia nigra protects against iron-dependent hydroxyl radical production under iron-accumulating conditions [15]. Studies with Ginkgolide B have shown to have an impact on the levels of ferroptosis markers such as reactive oxygen species, superoxide dismutase, malondialdehyde, reduced iron, glutathione peroxidase 4, nuclear receptor coactivator 4, ferritin heavy polypeptide 1, and acyl-CoA synthetase long-chain family member 4 in cerebral I/R injury [39]. Berberine decreases the effects of ferroptosis by decreasing reactive oxygen species, lipid peroxidation, and iron levels while increasing levels of glutathione peroxidases 4, glutathione, superoxide dismutase, and cystine/glutamate antiporter SLC7A11 [40].…”

Section: Iron Toxicitymentioning

confidence: 99%

On the Role of Iron in Idiopathic Parkinson’s Disease

Huenchuguala,

Segura-Aguilar

2023

Biomedicines

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The transition metal characteristics of iron allow it to play a fundamental role in several essential aspects of human life such as the transport of oxygen through hemoglobin or the transport of electrons in the mitochondrial respiratory chain coupled to the synthesis of ATP. However, an excess or deficiency of iron is related to certain pathologies. The maintenance of iron homeostasis is essential to avoid certain pathologies related to iron excess or deficiency. The existence of iron deposits in postmortem tissues of Parkinson’s patients has been interpreted as evidence that iron plays a fundamental role in the degenerative process of the nigrostriatal system in this disease. The use of iron chelators has been successful in the treatment of diseases such as transfusion-dependent thalassemia and pantothenate kinase-associated neurodegeneration. However, a clinical study with the iron chelator deferiprone in patients with Parkinson’s disease has not shown positive effects but rather worsened clinical symptoms. This suggests that iron may not play a role in the degenerative process of Parkinson’s disease.

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“…[68,69,70] Ginkgolide C Leaves mostly, root andAnti-inflammatory, antioxidant, anticancer, and antiadipogenesis properties [71,72]. …”

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confidence: 99%

“…[[65][66][67] Anti-inflammatory, antioxidant, antiplatelet aggregation, and anti-shock properties. [[68][69][70] Leaves mostly, root and bark. Anti-inflammatory, antioxidant, antiplatelet aggregation, and anti-shock properties [68][69][70].…”

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confidence: 99%

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Ginkgo biloba: A Leaf of Hope in the Fight against Alzheimer’s Dementia: Clinical Trial Systematic Review

Pagotto,

Santos,

Osman

et al. 2024

Antioxidants

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Alzheimer’s disease (AD) is a stealthy and progressive neurological disorder that is a leading cause of dementia in the global elderly population, imposing a significant burden on both the elderly and society. Currently, the condition is treated with medications that alleviate symptoms. Nonetheless, these drugs may not consistently produce the desired results and can cause serious side effects. Hence, there is a vigorous pursuit of alternative options to enhance the quality of life for patients. Ginkgo biloba (GB), an herb with historical use in traditional medicine, contains bioactive compounds such as terpenoids (Ginkgolides A, B, and C), polyphenols, organic acids, and flavonoids (quercetin, kaempferol, and isorhamnetin). These compounds are associated with anti-inflammatory, antioxidant, and neuroprotective properties, making them valuable for cognitive health. A systematic search across three databases using specific keywords—GB in AD and dementia—yielded 1702 documents, leading to the selection of 15 clinical trials for synthesis. In eleven studies, GB extract/EGb 761® was shown to improve cognitive function, neuropsychiatric symptoms, and functional abilities in both dementia types. In four studies, however, there were no significant differences between the GB-treated and placebo groups. Significant improvements were observed in scores obtained from the Mini-Mental State Examination (MMSE), Short Cognitive Performance Test (SKT), and Neuropsychiatric Inventory (NPI). While the majority of synthesized clinical trials show that Ginkgo biloba has promising potential for the treatment of these conditions, more research is needed to determine optimal dosages, effective delivery methods, and appropriate pharmaceutical formulations. Furthermore, a thorough assessment of adverse effects, exploration of long-term use implications, and investigation into potential drug interactions are critical aspects that must be carefully evaluated in future studies.

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Ginkgolide B attenuates cerebral ischemia-reperfusion injury via inhibition of ferroptosis through disrupting NCOA4-FTH1 interaction

Cited by 11 publications

References 43 publications

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

Ferritinophagy and Ferroptosis in Cerebral Ischemia Reperfusion Injury

On the Role of Iron in Idiopathic Parkinson’s Disease

Ginkgo biloba: A Leaf of Hope in the Fight against Alzheimer’s Dementia: Clinical Trial Systematic Review

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