The neuroprotective mechanisms of naringenin: Inhibition of apoptosis through the PI3K/AKT pathway after hypoxic-ischemic brain damage

Li, Luyao; Lin, Zhen; Yuan, Junhui; Li, Pingping; Wang, Qi; Cho, Namki; Wang, Yi; Lin, Zhenlang

doi:10.1016/j.jep.2023.116941

Cited by 7 publications

(3 citation statements)

References 87 publications

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“…Our data showed that miR-124 mimics significantly reduced mRNA levels of Caspase-3 and Bax, while increasing mRNA levels of Bcl-2 from a molecular perspective. This aligns with previous research confirming the impact of oxidative stress on neuronal apoptosis in HIBD, indicating that miR-124 overexpression suppresses oxidative stress, alleviating mitochondrial dysfunction and apoptosis in neurons after OGD/R treatment [41].…”

Section: Discussionsupporting

confidence: 92%

MicroRNA-124 negatively regulates STAT3 to alleviate hypoxic-ischemic brain damage by inhibiting oxidative stress

Geng,

Feng,

et al. 2024

Aging

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MicroRNA-124 (miR-124) is implicated in various neurological diseases; however, its significance in hypoxic-ischaemic brain damage (HIBD) remains unclear. This study aimed to elucidate the underlying pathophysiological mechanisms of miR-124 in HIBD. In our study performed on oxygen-glucose deprivation followed by reperfusion (OGD)/R-induced primary cortical neurons, a substantial reduction in miR-124 was observed. Furthermore, the upregulation of miR-124 significantly mitigated oxidative stress, apoptosis, and mitochondrial impairment. We demonstrated that miR-124 interacts with the signal transducer and activator of transcription 3 (STAT3) to exert its biological function using the dual-luciferase reporter gene assay. As the duration of OGD increased, miR-124 exhibited a negative correlation with STAT3 . STAT3 overexpression notably attenuated the protective effects of miR-124 mimics, while knockdown of STAT3 reversed the adverse effects of the miR-124 inhibitor. Subsequently, we conducted an HIBD model in rats. In vivo experiments, miR-124 overexpression attenuated cerebral infarction volume, cerebral edema, apoptosis, oxidative stress, and improved neurological function recovery in HIBD rats. In summary, the neuroprotective effects of the miR-124/STAT3 axis were confirmed in the HIBD model. MiR-124 may serve as a potential biomarker with significant therapeutic implications for HIBD.

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Section: Discussionsupporting

confidence: 92%

MicroRNA-124 negatively regulates STAT3 to alleviate hypoxic-ischemic brain damage by inhibiting oxidative stress

Geng,

Feng,

et al. 2024

Aging

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“…We measured brain water content using the standard wet–dry method at 24 and 72 h after ischemia 8,15 . The brains were swiftly deleted after the mice ( n = 6 per group per time point) were anesthetized with 10% chloral hydrate and euthanized.…”

Section: Methodsmentioning

confidence: 99%

“…We measured brain water content using the standard wet–dry method at 24 and 72 h after ischemia. 8 , 15 The brains were swiftly deleted after the mice ( n = 6 per group per time point) were anesthetized with 10% chloral hydrate and euthanized. The frontal lobe was sectioned off into 3‐mm‐thick coronal slices, and the halves were labeled as ipsilateral and contralateral hemispheres.…”

Section: Methodsmentioning

confidence: 99%

Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β

Zheng,

Zhang,

Dong

et al. 2023

Immunity Inflam & Disease

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ObjectiveTissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxidant, anti‐inflammatory, antiproliferative, and neuroprotective effects. In the present study, we explored the neuroprotective effects and potential mechanisms of Sal B after I/R injury.MethodsWe induced cerebral ischemia in male CD‐1 mice through transient (60 min) middle cerebral artery occlusion (tMCAO), and then injected Sal B (30 mg/kg) intraperitoneally. Neurological deficits, infarct volumes, and brain edema were assessed at 24 and 72 h after tMCAO. We detected the expression of Toll‐like receptor 4 (TLR4), phosphorylated‐p38 mitogen‐activated protein kinase (P‐p38 MAPK), phosphorylated c‐Jun amino (N)‐terminal kinases (p‐JNK), nuclear factor‐κB (NF‐κB), and interleukin‐1β (IL‐1β) in the brain tissue.ResultsCompared with the tMCAO group, Sal B significantly improved neurological deficits, reduced infarct size, attenuated cerebral edema, and downregulated the expression of pro‐inflammatory mediators TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β in brain tissue after I/R injury.ConclusionWe found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties.

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Phytochemicals: Promising Alternatives for Metabolic Regulation in Neurodegenerative Diseases

Kar,

Panda

2024

Altered Metabolism: A Major Contributor of Comorbidities in Neurodegenerative Diseases

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The neuroprotective mechanisms of naringenin: Inhibition of apoptosis through the PI3K/AKT pathway after hypoxic-ischemic brain damage

Cited by 7 publications

References 87 publications

MicroRNA-124 negatively regulates STAT3 to alleviate hypoxic-ischemic brain damage by inhibiting oxidative stress

MicroRNA-124 negatively regulates STAT3 to alleviate hypoxic-ischemic brain damage by inhibiting oxidative stress

Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β

Phytochemicals: Promising Alternatives for Metabolic Regulation in Neurodegenerative Diseases

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