ReferenceID 5182
EGCG protects the mouse brain against cerebral ischemia/reperfusion injury by suppressing autophagy via the AKT/AMPK/mTOR phosphorylation pathway
Front Pharmacol
Stroke remains one of the leading reasons of mortality and physical disability worldwide. The treatment of cerebral ischemic stroke faces challenges, partly due to a lack of effective treatments. In this study, we demons
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 5182
- Evidence Id
- 21772
- Core Evidence Id
- 21772
- Source Reference Id
- 3648
- Herb2 Reference Id
- HBREF004445
- Subject Paper Key
- HBIN025346_36147330
- Pubmed Id
- 36147330
- Doi
- 10.3389/fphar.2022.921394
- Paper Title
- EGCG protects the mouse brain against cerebral ischemia/reperfusion injury by suppressing autophagy via the AKT/AMPK/mTOR phosphorylation pathway
- Paper Abstract
- Stroke remains one of the leading reasons of mortality and physical disability worldwide. The treatment of cerebral ischemic stroke faces challenges, partly due to a lack of effective treatments. In this study, we demonstrated that autophagy was stimulated by transient middle cerebral artery occlusion/reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R). Treatment with (-)-epigallocatechin-3-gallate (EGCG), a bioactive ingredient in green tea, was able to mitigate cerebral ischemia/reperfusion injury (CIRI), given the evidence that EGCG administration could reduce the infarct volume and protect poststroke neuronal loss in MCAO/R mice in vivo and attenuate cell loss in OGD/R-challenged HT22 cells in vitro through suppressing autophagy activity. Mechanistically, EGCG inhibited autophagy via modulating the AKT/AMPK/mTOR phosphorylation pathway both in vivo and in vitro models of stroke, which was further confirmed by the results that the administration of GSK690693, an AKT/AMPK inhibitor, and rapamycin, an inhibitor of mTOR, reversed aforementioned changes in autophagy and AKT/AMPK/mTOR signaling pathway. Overall, the application of EGCG relieved CIRI by suppressing autophagy via the AKT/AMPK/mTOR phosphorylation pathway.
- Journal
- Front Pharmacol
- Publish Year
- 2022
- Experiment Subject
- mouse; ogd/r-challenged ht22 cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Stroke; Cerebral Ischemic Stroke; Physical Disability; Cerebral Ischemia/reperfusion Injury
- Paper Title Cn
- Paper Title En
- EGCG protects the mouse brain against cerebral ischemia/reperfusion injury by suppressing autophagy via the AKT/AMPK/mTOR phosphorylation pathway
- Bilingual Status
- semi_complete