Repository of Research and Investigative Information

Repository of Research and Investigative Information

Ilam University of Medical Sciences

Tannic acid protects aged brain against cerebral hypoperfusion via modulation of Nrf2 and inflammatory pathways

Fri Mar 29 14:39:01 2024

(2021) Tannic acid protects aged brain against cerebral hypoperfusion via modulation of Nrf2 and inflammatory pathways. Neuroscience Letters. p. 6. ISSN 0304-3940

Full text not available from this repository.

Official URL: http://apps.webofknowledge.com/InboundService.do?F...

Abstract

Current study purposed to investigate the neuroprotective effects of Tannic Acid (TA) on mild chronic cerebral hypoperfusion model in rats. Male Wistar rats were subjected to permanent Unilateral Common Carotid Artery Occlusion (UCCAO), followed by TA treatment (0.05 w/v) in drinking water for one month. Nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H: quinone oxidoreductase 1 (NQO-1), heme oxygenase-1 (HO-1), factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), tumor necrosis factor-alpha (TNF-alpha), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3, blood triglyceride, blood glucose, and liver enzymes' activity were detected after the experimental period. Also, behavioral tests, hematoxylin and eosin (H&E) staining, and PET scan were performed after treatment. Post-treatment of TA improved locomotion and memory function (P < 0.001), and reduced neural cell death (P < 0.001) in the treatment group compared to UCCAO rats. Furthermore, long-term TA treatment significantly increased the levels of Nrf2 (P < 0.001), NQO-1 (P < 0.001), and HO-1 (P < 0.001) in the hippocampus of the treatment group compared to the UCCAO group. TA consumption in the treatment group applied its anti-inflammatory effects via reducing the activity of NF-kappa B and TNF alpha in comparison with the UCCAO group (P 0.001 for both). Blood triglyceride, blood glucose, and liver enzymes did not change considerably in the groups (P 0.05). The current results indicate that long-term posttreatment of TA exhibits protective effects against memory deficit and motor dysfunction. The cellular mechanism of TA in hypoperfused rats might be associated with the activation of antioxidant pathways, especially the Nrf2 pathway, and suppressing inflammatory factors like NF-kappa B and TNF-alpha.

Item Type: Article
Creators:
CreatorsEmail
Sehati, F.UNSPECIFIED
Ahmadi, I.UNSPECIFIED
Farivar, N.UNSPECIFIED
Ranjbaran, M.UNSPECIFIED
Sadat-Shirazi, M. S.UNSPECIFIED
Nabavizadeh, F.UNSPECIFIED
Shavakandi, S. M.UNSPECIFIED
Ashabi, G.UNSPECIFIED
Keywords: Tannic acid Nrf2 Cerebral hypoperfusion Ischemia Apoptosis Rat antioxidants dementia damage Neurosciences & Neurology
Divisions:
Page Range: p. 6
Journal or Publication Title: Neuroscience Letters
Journal Index: ISI
Volume: 765
Identification Number: https://doi.org/10.1016/j.neulet.2021.136263
ISSN: 0304-3940
Depositing User: مهندس مهدی شریفی
URI: http://eprints.medilam.ac.ir/id/eprint/3714

Actions (login required)

View Item View Item