Dietary supplementation with N-acetyl cysteine, a-tocopherol and a-lipoic acid reduces the extent of oxidative stress and proinflammatory state in aged rat brain

Ishita Guha Thakurta, Mrittika Chattopadhyay, Arindam Ghosh, Sasanka Chakrabarti

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

Abstract The present study has attempted to understand how oxidative stress contributes to the development of proinflammatory state in the brain during aging. Three groups of rats have been used in this study: young (4-6 months, Group I), aged (22-24 months, Group II) and aged with dietary antioxidant supplementation (Group III). The antioxidants were given daily from 18 months onwards in the form of a combination of N-acetyl cysteine (50 mg/100 g body weight), a-lipoic acid (3 mg/100 g body weight), and a-tocopherol (1.5 mg/100 g body weight) till the animals were used for the experiments between 22 and 24 months. Several measurements have been made to evaluate the ROS (reactive oxygen species) production rate, the levels of proinflammatory cytokines (IL-1b, IL-6 and TNF-α) and the activation status ofNF-κb (p65 subunit) in brain of the three groups of rats under the study. Our results reveal that brain aging is accompaniedwith a significant increase in NADPH oxidase activity and mitochondrial ROS production, a distinct elevation of IL-1β, IL-6 and TNF-α levels along with increased nuclear translocation of NF-κb (p65 subunit) and all these phenomena are partially but significantly prevented by the long-term dietary antioxidant treatment. The results imply that chronic dietary antioxidants by preventing oxidative stress and proinflammatory statemay produce beneficial effects against multiple age-related deficits of the brain.

Original languageEnglish
Pages (from-to)479-488
Number of pages10
JournalBiogerontology
Volume13
Issue number5
DOIs
StatePublished - Oct 2012
Externally publishedYes

Keywords

  • Antioxidants
  • Brain aging
  • Mitochondrial ROS
  • NADPH oxidase
  • NF-κb
  • Proinflammatory cytokines

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