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Influence of eugenol on oxidative stress biomarkers in the liver of carrageenan-induced arthritis rats.

Stephen Adeniyi AdefeghaSunday I OyeleyeBathlomew Maduka OkekeGaniyu Oboh
Published in: Journal of basic and clinical physiology and pharmacology (2018)
Background Eugenol is the foremost constituent of clove oil and widely distributed in many plants. It possesses many pharmaceutical applications, including antioxidant, anti-inflammatory, and anti-tumorigenic properties, among others. This study evaluates the influence of eugenol on oxidative stress biomarkers in the liver of carrageenan-induced arthritis (CIA) rats. Methods Sixty albino rats were randomly divided into 10 (n=6) groups. Group I is the control group that received saline solution orally. Groups II and VII rats received 2.5 mg/kg of eugenol orally (EUG-2.5). Rats in groups III/VIII and IV/IX received 5 and 10 mg/kg of eugenol orally (EUG-5 and EUG-10), respectively. Groups V and X received 0.2 mg/kg of dexamethasone (DEX-0.2) orally. Groups VI to X were injected with 1% carrageenan intra-articularly. Behavioral studies were conducted after 21 days of treatment. Thereafter, the animals were sacrificed, and the livers were isolated and used for biochemical analysis. Results Reduced body weight in arthritic rats was recorded compared to normal controls. Reduced tibiofemoral joint edema and increased spontaneous movement were observed in CIA rats with decreased superoxide dismutase, catalase, reduced glutathione (GSH), glutathione peroxidase, and GSH S-transferase activities compared with the normal control group. Increased endogenous enzyme activities and decreased elevated lipid peroxidation were also observed after eugenol treatment. Conclusion Eugenol ameliorates carrageenan-induced oxidative stress in the liver of arthritic rats.
Keyphrases
  • oxidative stress
  • rheumatoid arthritis
  • anti inflammatory
  • body weight
  • dna damage
  • hydrogen peroxide
  • low dose
  • high glucose
  • endothelial cells
  • endoplasmic reticulum stress
  • induced apoptosis