Article detail · 2025
Therapeutic role of melatonin on acrylamide-induced neurotoxicity via reducing ER stress, inflammation, and apoptosis in a rat model
Journal
BMC Pharmacology and ToxicologyISSN 0882-4010
The ISSN points to another catalog journal; the name is from the YÖKSİS record.
- Year
- 2025
- Type
- article
Data source split
- YÖKSİS YÖKSİS article record
- YÖKSİS venue BMC Pharmacology and Toxicology
- Catalog match (ISSN) Microbial Pathogenesis
- OpenAlex OpenAlex enrichment (abstract, citations, topics)
Abstract
OpenAlex · English
This study examined the antioxidant, anti-inflammatory, and neuroprotective effects of melatonin (MEL) against acrylamide (ACR)-induced neurotoxicity in Sprague-Dawley rats. The experimental groups included control, ACR, MEL10+ACR, MEL20+ACR, and MEL20. MEL at doses of 10 and 20 mg/kg, and ACR at 50 mg/kg, were administered intraperitoneally for 14 days. On the 15th day, locomotor activity was assessed, and brain tissues were analyzed biochemically, molecularly, and histopathologically. ACR exposure decreased locomotor activity, increased malondialdehyde (MDA) and reduced glutathione (GSH) levels, indicating oxidative stress, and decreased antioxidant enzyme activities (SOD, GPx, CAT). High-dose MEL (MEL20+ACR) effectively reduced lipid peroxidation and restored antioxidant enzyme activities. MEL treatment also suppressed proinflammatory cytokines (TNF-α, IL-1β, IL-6) and neuronal nitric oxide synthase (nNOS), demonstrating anti-inflammatory effects. Furthermore, MEL mitigated ACR-induced neurotoxicity by reducing acetylcholinesterase (AChE) and monoamine oxidase (MAO) levels. ER stress markers (GRP78, ATF4, ATF6, sXBP1, CHOP) and apoptotic markers (Bax, Caspase-3) were elevated following ACR exposure but were suppressed by MEL. Additionally, MEL reduced ACR-induced increases in 8-hydroxy-2-deoxyguanosine (8-OHdG) and glial fibrillary acidic protein (GFAP), markers of DNA damage and astrocyte activation, respectively. These findings underscore the potential of MEL to counteract ACR-induced neurotoxicity through its comprehensive antioxidant, anti-inflammatory, and neuroprotective actions.
Topics
Citations
OpenAlex cited_by_count. Not a WoS or Scopus citation count; those sources have no separate column here.
12 citations
OpenAlex cited_by_count (cache / database)
14 publications in the local catalog that cite this work (OpenAlex reference match; not the full global list).
- Protective effects of naringin against oxidative stress, inflammation, apoptosis, and DNA damage in rats with doxorubicin-induced hepatotoxicity 2025
- Protective effects of naringin against oxidative stress, inflammation, apoptosis, and DNA damage in rats with doxorubicin-induced hepatotoxicity 2025
- Protective effects of naringin against oxidative stress, inflammation, apoptosis, and DNA damage in rats with doxorubicin-induced hepatotoxicity 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025
- Protective Effect of Curcumin Against the Toxic Effect of Acrylamide on the Rat Hippocampus 2025