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- W2912745536 abstract "Hypoxic-ischemic encephalopathy (HIE) is detrimental to newborns and is associated with high mortality and poor prognosis. Thus, the primary aim of the present study was to determine whether glycine could (1) attenuate HIE injury in rats and hypoxic stress in PC12 cells and (2) downregulate mitochondria-mediated autophagy dependent on the adenosine monophosphate- (AMP-) activated protein kinase (AMPK) pathway. Experiments conducted using an in vivo HIE animal model and in vitro hypoxic stress to PC12 cells revealed that intense autophagy associated with mitochondrial function occurred during in vivo HIE injury and in vitro hypoxic stress. However, glycine treatment effectively attenuated mitochondria-mediated autophagy. Additionally, after identifying alterations in proteins within the AMPK pathway in rats and PC12 cells following glycine treatment, cyclosporin A (CsA) and 5-aminoimidazole-4-carboxamide-1-b-4-ribofuranoside (AICAR) were administered in these models and indicated that glycine protected against HIE and CoCl 2 injury by downregulating mitochondria-mediated autophagy that was dependent on the AMPK pathway. Overall, glycine attenuated hypoxic-ischemic injury in neurons via reductions in mitochondria-mediated autophagy through the AMPK pathway both in vitro and in vivo ." @default.
- W2912745536 created "2019-02-21" @default.
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- W2912745536 date "2019-02-06" @default.
- W2912745536 modified "2023-10-15" @default.
- W2912745536 title "Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway" @default.
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- W2912745536 doi "https://doi.org/10.1155/2019/4248529" @default.
- W2912745536 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6381570" @default.
- W2912745536 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30881590" @default.
- W2912745536 hasPublicationYear "2019" @default.
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