Journals / Journal of Cellular Neuroscience and Oxidative Stress / 2025 / Volume: 17 Issue: 2

Neuroprotective Effects of Vitamin C and Vitamin E on Oxidative Stress in Rats with Scopolamine-Induced Dementia

Pages
1252–1260
Publication Date
2025-10-07
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In conclusion, the results suggest that both vitamins exhibited neuroprotective properties by ameliorating oxidative stress and improving cognitive outcomes in dementia rats.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive, behavioural, and personality declines.
📊
Key Findings & Data:After seven days of treatment with vitamins C and E, AD was induced in the rats on day eight by the injection of 4 mg/kg body weight of scopolamine.
💡
Conclusion & Impact:In conclusion, the results suggest that both vitamins exhibited neuroprotective properties by ameliorating oxidative stress and improving cognitive outcomes in dementia rats.
🔬Design:Text.Serial.Journal
📍Scope:Comprehensive Sample
⚙️Variables:Alzheimer · cognitive function · dementia

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that causes cognitive, behavioural, and personality declines. In the etiology of AD, oxidative stress has a main role. This study was carried out to investigate the neuroprotective effects of vitamins C and E on cognitive function and oxidative stress in rats with scopolamine-induced AD. After seven days of treatment with vitamins C and E, AD was induced in the rats on day eight by the injection of 4 mg/kg body weight of scopolamine. Behavioural outcomes such as anxiety, learning and memory were carried out using an elevated plus-maze, and novel object recognition tasks. Malondialdehyde (MDA), antioxidant enzymes, and vitamins were assessed in the brain tissue. Vitamins C and E treatment enhanced memory and behavioural functions in dementia rats when compared with the control group. The results also showed that the vitamin C and vitamin E treated groups had higher brain levels of vitamin C and vitamin E compared to the control group. Furthermore, both treatments reduced the MDA levels compared to the control group. The group that received either of the vitamins indicated higher superoxide dismutase and catalase activities compared to the control group. In conclusion, the results suggest that both vitamins exhibited neuroprotective properties by ameliorating oxidative stress and improving cognitive outcomes in dementia rats.

🔖

Cite This Article

Muhammad, S. A., Aliyu, A. D., Abolaji, A. O., Jiyah, A., Bulama, I., Ibrahim, A., Abbas, A., Imam, M. U., Bilbis, L. (2025). Neuroprotective Effects of Vitamin C and Vitamin E on Oxidative Stress in Rats with Scopolamine-Induced Dementia. Journal of Cellular Neuroscience and Oxidative Stress, Volume: 17 Issue: 2, 1252–1260. https://doi.org/10.37212/jcnos.1741523

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Adiguzel C, Kalender Y. (2020). Bendiocarb-induced nephrotoxicity in rats and the protective role of vitamins C and E. Environ Sci Pollut Res Int. 27(6):6449–6458. https://doi.org/10.1007/s11356-019-07260-x.
  2. Beers RF, Sizer IW. (1952). A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. J Biol Chem. 195(1):133–140.
  3. Beydoun MA, Canas JA, Fanelli-Kuczmarski MT, Maldonado AI, Shaked D, Kivimaki M, Evans MK, Zonderman AB. (2020). Association of antioxidant vitamins A, C, E and carotenoids with cognitive performance over time: a cohort study of middle-aged adults. Nutrients. 12(11):3558. https://doi.org/10.3390/nu12113558.
  4. Bilbis LS, Muhammad SA, Saidu Y, Adamu Y. (2012).
  5. Effect of vitamins A, C, and E supplementation in the treatment of metabolic syndrome in albino rats. Biochem Res Int. 2012: 678582. https://doi.org/10.1155/2012/678582.
  6. Buccellato FR, D’Anca M, Fenoglio C, Scarpini E, Galimberti D. (2021). Role of oxidative damage in Alzheimer’s disease and neurodegeneration: from pathogenic mechanisms to biomarker discovery. Antioxidants. 10(9):1353. https://doi.org/10.3390/antiox10091353.
  7. Cook-Mills JM, McCary CA. (2010). Isoforms of vitamin E differentially regulate inflammation. Endocr Metab Immune Disord Drug Targets. 10(4):348–366. https://doi.org/10.2174/1871530311006040348.
  8. Dias-Santagata D, Fulga TA, Duttaroy A, Feany MB. (2007). Oxidative stress mediates tau-induced neurodegeneration in Drosophila. J Clin Invest. 117(1):236–245. https://doi.org/10.1172/JCI28769.
  9. Fariss MW, Zhang J-G. (2003). Vitamin E therapy in Parkinson’s disease. Toxicology. 189(1–2):129–146. https://doi.org/10.1016/s0300-483x(03)00158-6.
  10. Getoff N. (2013). Vitamin C: electron emission, free radicals and biological versatility. In Vivo. 27(5):565–570.
  11. Gloria AN, Nnabuihe ED. (2024). Protective effects of vitamin C and E on hippocampus of methamphetamine induced brain disorder in adult male Wistar rats. World J Pharm Res. 13(9):1612–1662. D’souza D, Subhas BG, Shetty SR, Balan P. (2012). Estimation of serum malondialdehyde in potentially malignant disorders and post-antioxidant treated patients: A biochemical study. Contemp Clin Dent 3(4):448-451. https://doi.org/10.4103/0976-237X.107438
  12. Handley SL, Mithani S. (1984). Effects of alpha-adrenoceptor agonists and antagonists in a maze-exploration model of ‘fear’-motivated behaviour. Naunyn Schmiedebergs Arch Pharmacol. 327(1):1–5. https://doi.org/10.1007/BF00504983.
  13. Harrison FE, Hosseini AH, Dawes