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Acetyl‐L‐carnitine‐mediated neuroprotection during hypoxia is attributed to ERK1/2‐Nrf2‐regulated mitochondrial biosynthesis by Kalpana Barhwal Hota; Sunil Kumar Hota; Om Prakash Chaurasia; Shashi Bala Singh is a Neuroscience article available to read on EtoBox.
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## Abstract Neuronal damage in hypoxia and several neurodegenerative disorders is invariably associated with oxidative damage and mitochondrial dysfunction. Administration of acetyl‐L‐carnitine (ALCAR) on the other hand attenuates neuronal damage, prevents apoptosis, and improves energy status in hypoxic stress through less understood mechanisms. Becasue mitochondrial biogenesis could be a possible mechanism for ALCAR‐induced improvement in bioenergetics in neurons, the present study aimed at exploring signaling pathways of ALCAR‐induced neuroprotection in hypoxia and possible occurrence of mitochondrial biogenesis. To create global hypoxia, adult Sprague–Dawley rats were exposed to a simulated altitude of 7,620 m at standard temperature and humidity conditions. We here demonstrate that administration of ALCAR to hypoxic rats for a period of 2 weeks effectively protected hippocampal neurons from mitochondrial dysfunction, excitotoxicity, and neurodegeneration. ALCAR administration resulted in peroxisome proliferator‐activated receptor γ coactivator‐1α and nuclear respiratory factor‐1‐induced mitochondrial biogenesis, the expression of which was regulated by an extracellular‐related
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It is typically read by researchers, students, and practitioners in Neuroscience.
- Author
- Kalpana Barhwal Hota; Sunil Kumar Hota; Om Prakash Chaurasia; Shashi Bala Singh
- Publisher
- Wiley
- Published
- 2011
- Language
- EN
- Field
- Neuroscience (Life Sciences)
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