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Theragra chalcogramma Hydrolysates, Rich of Fragment Gly-Leu-Pro-Ser-Tyr-Thr, Ameliorate Alcohol-Induced Cognitive Impairment via Attenuating Neuroinflammation and Enhancing Neuronal Plasticity in Sprague-Dawley Rats.

Abstract
Chronic alcohol abuse induces the cognitive deficits and is associated with low-grade inflammation and neurodegeneration. Currently, by virtue of the immunomodulatory and neuroprotective properties, nutrients represent a promising strategy to attenuate cognitive impairments. We previously prepared the hydrolysates from Theragra chalcogramma skin (TCH), and this study aims to evaluate the neuroprotection of TCH on alcohol-induced cognitive impairment (AICI) and to elucidate the associated mechanism. Behavioral results showed that TCH effectively ameliorated AICI and this amelioration was highly associated with the decrease of IL-1β and the increase of BDNF, CREB, and PSD95 in AICI rats (P < 0.05). Furthermore, TCH restored the histopathological impairment in hippocampus by reactivating extracellular signal-regulated kinase and suppressing Caspase-3 apoptosis signal pathways and modulating the abnormality of neurotransmitters acetylcholine and γ-aminobutyric acid(P < 0.05 or 0.01). Therefore, TCH exhibits potent attenuation of neuroinflammation and represents a potential ingredient for prevention of AICI.
AuthorsDefeng Xu, Mouming Zhao
JournalJournal of agricultural and food chemistry (J Agric Food Chem) Vol. 70 Issue 39 Pg. 12513-12524 (Oct 05 2022) ISSN: 1520-5118 [Electronic] United States
PMID36162996 (Publication Type: Journal Article)
Chemical References
  • Brain-Derived Neurotrophic Factor
  • Dipeptides
  • prolyl-serine
  • Ethanol
  • gamma-Aminobutyric Acid
  • glycylleucine
  • Extracellular Signal-Regulated MAP Kinases
  • Caspase 3
  • Acetylcholine
Topics
  • Acetylcholine (metabolism)
  • Animals
  • Brain-Derived Neurotrophic Factor (metabolism)
  • Caspase 3 (metabolism)
  • Cognitive Dysfunction (drug therapy, metabolism)
  • Dipeptides
  • Ethanol (adverse effects, metabolism)
  • Extracellular Signal-Regulated MAP Kinases (metabolism)
  • Hippocampus
  • Neuroinflammatory Diseases
  • Neuronal Plasticity
  • Rats
  • Rats, Sprague-Dawley
  • gamma-Aminobutyric Acid (metabolism)

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