ArticleExperimental and therapeutic medicine2021
Hypoxic postconditioning-induced neuroprotection increases neuronal autophagy via activation of the SIRT1/FoxO1 signaling pathway in rats with global cerebral ischemia.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.Cell death discovery · 2024Review
- Exercise postconditioning reduces ischemic injury via suppression of cerebral gluconeogenesis in rats.Brain and behavior · 2023Article
- How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway.AIMS neuroscience · 2023Article
- A novel link between silent information regulator 1 and autophagy in cerebral ischemia-reperfusion.Frontiers in neuroscience · 2022Review
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9 authors at 1 institution in 1 country.
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Abstract
Hypoxic postconditioning (HPC) has been reported to be a beneficial and promising treatment for global cerebral ischemia (GCI). However, its neuroprotective mechanism remains unclear. The aim of the present study was to determine whether the protective effects of HPC in a rat model of GCI were due to the upregulation of autophagy via the silent information regulator transcript-1 (SIRT1)/Forkhead box protein 1 (FoxO1) pathway. Morris water maze test revealed that HPC attenuated cognitive damage in GCI rats. HPC also significantly increased the levels of the autophagy-related protein LC3-II, SIRT1 and FoxO1 compared with those in the GCI group. However, the HPC-induced LC3-II upregulation was blocked by the SIRT1 inhibitor EX527. These results suggested that the beneficial effects of HPC on GCI rats were due to the upregulation of ischemiainduced autophagy and involved the SIRT1/FoxO1 signaling pathway.
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