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Neuroprotective effects of resveratrol against β ‐amyloid induced oxidative damage and memory loss in rat hippocampal (H19‐7) cells (647.44)
Author(s) -
Rege Shraddha,
Bottcher Mary,
Geetha Thangiah,
Broderick Tom,
Babu Jeganathan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.647.44
Subject(s) - neuroprotection , resveratrol , chemistry , oxidative stress , glutathione reductase , pharmacology , biochemistry , glutathione peroxidase , antioxidant , superoxide dismutase , glutathione , biology , enzyme
Resveratrol is a polyphenolic phytoalexin known to exhibit neuroprotective effects in several experimental models. Accumulation of amyloid beta in the Alzheimer disease patient brain seems to be the cause of cognitive impairment and neuronal loss. The present study evaluates the neuroprotective action of resveratrol on β‐amyloid induced oxidative stress and memory loss in cultured rat hippocampal H19‐7 neuronal cell line pretreated with 75 μM of resveratrol for 2 hrs followed by 25 μM of Aβ (1‐40) for 24 hrs. The lipid peroxidase levels were significantly increased in amyloid β treated H19‐7 cells. The enzymic antioxidants like superoxide dismutase, catalase, glutathione reductase, and non‐enzymic antioxidants like tocopherol, ascorbic acid and glutathione were decreased. amyloid β treatment also increased tau phosphorylation and decreased expressions of certain proteins like Insulin Degrading Enzyme (IDE), glycogen synthase kinase 3beta and p62, which are involved in Amyloid beta degradation and PSD‐95, Arc proteins essential for synaptic maturity and plasticity. Resveratrol treatment attenuated the lipid peroxide levels, up‐regulated the antioxidant activities and increased the expression of proteins involved in neuroprotection in H19‐7 cells. These findings suggest the neuroprotective effect of resveratrol in improving the β‐ amyloid induced oxidative damage and memory loss in vitro.

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