Gomisin N attenuated cerebral ischemia-reperfusion injury through inhibition of autophagy by activating the PI3K/AKT/mTOR pathway

Li, Ruoqi; Zheng, Yingyi; Zhang, Jiaxue; Zhou, Yuan; Fan, Xiang

doi:10.1016/j.phymed.2023.154644

Cited by 6 publications

(1 citation statement)

References 39 publications

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“…As PI3K/AKT/mTOR and PI3K III/Beclin-1/Bcl-2 are important signaling pathways involved in autophagy. Activate the signaling pathway of PI3K/AKT/mTOR can inhibits the autophagy of a variety of cells [20][21][22][23] . While Beclin-1 is a speci c autophagy gene in the PI3K III/Beclin-1/Bcl-2 signaling pathway, beclin-1 protein can form a compound with PI3K III to induce related autophagy proteins locate on the autophagosome membrane, thus promote the formation of autophagosomes [24] .…”

Section: Discussionmentioning

confidence: 99%

Hypothermia prevents OGD/R induced injury by activating the PI3K/AKT/mTOR signaling pathway and enhancing autophagy

Shi,

Gao,

Wang

et al. 2024

Preprint

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Objectives To evaluate the role of hypothermia in the injury of PC12 cells which induced by OGD/R. To investigate the mechanism of hypothermia intervention to alleviate OGD/R-induced injury of PC12 cells through phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway and autophagy, and to lay a foundation and provide theoretical basis for clinical application of hypothermia on protect nerve injury in the future. Methods Induce PC12 cells establish an Ischemia reperfusion injury model in vitro by OGD/R. Then, intervene PC12 cells with OGD/R and OGD/R treated with LY294002 inhibitor at 37℃, 32℃, 27℃. Valuate cell viability by CCK-8 assay, detect the phosphorylation levels of PI3K, AKT and mTOR proteins through western blotting, evaluate signaling pathway activation of PI3K/AKT/mTOR, detect protein expression of LC3I/II by immunofluorescence and western blotting, and observe the autophagosomes by fluoroscopic electron microscopy to evaluate autophagy. Detect apoptosis by flow cytometry, and evaluate the cell damage. Results Hypothermia treatment could effectively improve the cell viability of PC12 cells treated with OGD/R, and the cell viability increased with the decrease of temperature (P < 0.05). Hypothermia treatment also promoted the increase of the phosphorylation levels of PI3K, AKT and mTOR proteins in cells (P < 0.05). In addition, flow cytometry was used to detect the apoptosis rate of different treatments, and the results showed that hypothermia could inhibit the apoptosis that induced by OGD/R. In the control group, OGD/R group and LY294002 inhibitor group, autophagy specific protein LC3I/II which labeled with green fluorescently was increased significantly under the culture conditions of 32℃ and 27℃, and the fluorescence signal was enhanced. Meanwhile, the expression level of LC3I/II also increased. Autophagosome was increased under the electron microscopy. Conclusion Hypothermia can inhibit apoptosis by regulating the PI3K/AKT/mTOR axis and the level of autophagy, thus protecting PC12 cell damage that induced by OGD/R.

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Section: Discussionmentioning

confidence: 99%

Hypothermia prevents OGD/R induced injury by activating the PI3K/AKT/mTOR signaling pathway and enhancing autophagy

Shi,

Gao,

Wang

et al. 2024

Preprint

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Voacangine protects hippocampal neuronal cells against oxygen–glucose deprivation/reoxygenation‐caused oxidative stress and ferroptosis by activating the PI3K‐Akt‐FoxO signaling

Li,

Sun,

Wang

et al. 2024

J of Applied Toxicology

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Voacangine, a naturally occurring alkaloid, has been testified to display beneficial effects on a variety of human diseases, but its role in ischemic stroke is unclear. The impacts of voacangine on oxygen–glucose deprivation/reoxygenation (OGD/R)‐tempted hippocampal neuronal cells are investigated. The bioinformatics analysis found that voacangine is a bioactive ingredient that may have good effects on ischemic stroke. KEGG pathways analysis found that voacangine may regulate ischemic stroke through modulating the PI3K‐Akt‐FoxO signaling pathway. Voacangine could mitigate OGD/R‐tempted cytotoxicity in HT22 cells. Voacangine mitigated OGD/R‐tempted oxidative stress in HT22 cells by diminishing reactive oxygen species level and enhancing superoxide dismutase level. Voacangine mitigated OGD/R‐tempted ferroptosis in HT22 cells. Voacangine promoted activation of the PI3K‐Akt‐FoxO signaling in OGD/R‐induced HT22 cells. Inactivation of the PI3K‐Akt‐FoxO signaling pathway reversed the protective effects of voacangine against OGD/R‐tempted oxidative stress, cytotoxicity, and ferroptosis in HT22 cells. In conclusion, voacangine protects hippocampal neuronal cells against OGD/R‐caused oxidative stress and ferroptosis by activating the PI3K‐Akt‐FoxO signaling.

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Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy

Zheng,

Jiang,

et al. 2024

Mol Neurobiol

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Gomisin N attenuated cerebral ischemia-reperfusion injury through inhibition of autophagy by activating the PI3K/AKT/mTOR pathway

Cited by 6 publications

References 39 publications

Hypothermia prevents OGD/R induced injury by activating the PI3K/AKT/mTOR signaling pathway and enhancing autophagy

Hypothermia prevents OGD/R induced injury by activating the PI3K/AKT/mTOR signaling pathway and enhancing autophagy

Voacangine protects hippocampal neuronal cells against oxygen–glucose deprivation/reoxygenation‐caused oxidative stress and ferroptosis by activating the PI3K‐Akt‐FoxO signaling

Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy

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