Role of Omega-3 in ameliorating acute liver injury-induced by D-galactose on adult male rats

Abstract

Background and objective: Numerous morphological and functional changes in the liver are linked to aging. The two main ageing processes that can cause significant damage to mitochondrial DNA and ultimately apoptosis are now well recognised to be inflammatory reaction and oxidative stress. Because aging is a poor prognostic factor that raises the mortality rate, it may also raise the risk of developing a number of liver illnesses. In rodents, chronic D-galactose treatment accelerates aging.In addition to improving hepatic beta oxidation and decreasing endogenous lipid production, omega-3 polyunsaturated fatty acids also have a positive effect on the metabolism of lipids and insulin sensitivity. They can also lower oxidative stress and hepatic inflammation, which merely lessens the damaging aging effect of D-galactose on rats.Methods: Four equal groups of twenty-eight (28) male Rattus norvegicus rats, weighing between 210 and 240 g, were randomly selected. Group T1 animals received an intraperitoneal injection of normal saline, while group T2 animals received an IP injection of D-galactose (150 mg/kg bwt) and were drenched 80 mg/kg (bwt) of Omega3 twice a day for 75 days. T3 received an intraperitoneal (I/P) injection of D-galactose (150 mg/kg b.wt) for 75 days, and they were drenched omega 3 (80 mg/kg b.wt) twice a day for 21 days. D-galactose (150 mg/kg b.wt) was given intraperitoneally (I/P) into T4 rats for 75 days. All animals have been sacrificed 24 hours after the last dose, and samples of liver tissue were obtained to look for histopathological changes, serum samples were gathered also for biochemical analysis.Conclusion: Omega-3 supplement for 75 days cause a significant enhancement with mitigating the aging harmful properties of D-galactose on liver functions and oxidative stress marker MDA and showing liver tissue sections showing the improvement with liver architecture occurring due to Omega 3 supplementation.