Immunomodulatory and Antioxidant Effects of Eugenol on Aluminium Chloride-Induced Neurotoxicity in Wistar Rats

Abstract

Aluminium and its compounds when taken orally can have negative impacts on a variety of enzymes leading to neurotoxicity. Apurinic endonuclease 1 (APE-1), a protein that performs multiple functions, including deoxyribonucleic acid (DNA) repair, is essential for cell survival. Thus, the determination of APE-1 with aluminium chloride (AlCl3) induced neuro-inflammation in Wistar rats was performed in this study. Wistar rats were divided into four groups, each with six animals. Group 1 received 100 mg/kg AlCl3 orally, Group 2 received 150 mg/kg eugenol, Group 3 received both 100 mg/kg AlCl3 and 150 mg/kg eugenol, and Group 4 received 0.8 ml/kg distilled water. Rats were euthanized after eight weeks, and brain tissues were homogenized and analysed. Oral administration of AlCl3 resulted in significant (p<0.01) decreased APE-1, superoxide dismutase (SOD) and amyloid beta-40 (Aβ-40), and significant (p<0.01) increased tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1), inducible nitric oxide synthase (iNOS), myeloperoxidase, and nitric oxide (NO). Co-administration of AlCl3 and eugenol significantly increased (p<0.01) APE-1, Aβ-40 and SOD, while significantly decreasing (p<0.01) TNF-α, IL-1, iNOS and MPO levels. Our findings suggest that eugenol, by targeting these most potent hallmarks of neurodegeneration could be an effective alternative in its treatment.