In rats fed a lot of fructose, which normally causes liver fat buildup and oxidative stress, giving the peptide thymosin‑alpha‑1 for 10 days brought many of those harmful changes back toward normal, lowering liver damage markers and inflammation and protecting liver cells.

The aim of this study was to investigate the effects of thymosin alpha(1) (Talpha(1)) in rats having fructose-induced steatosis. Fructose leads to experimental steatosis in the liver by exerting its effect on some components of the oxidant/antioxidant system, and on several cytokines (interleukin-1beta, -2, and -6) in blood. Twenty-four rats at random were divided into three groups (each group containing eight animals); the control group (C), which received a purified diet; the high-fructose-fed group (F); and the high-fructose-fed and Talpha(1) injected group (F + T). After the experimental period of 10 days, liver lipid peroxidation and antioxidant status, and blood IL-1beta, IL-2, and IL-6 levels were quantified. In comparison with the C group, the F group had a higher nitric oxide (NO) level, xanthine oxidase (XO) activity, and lipid peroxidation, as indicated by concentrations of thiobarbituric acid reactive substances (TBARS), and lower superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the liver. In the F + T group, these markers were near the values of the control group. In addition, increased IL-1beta and IL-6 levels were kept at near to normal levels with treatment of Talpha(1), but not IL-2 levels. In the F group, the most consistent findings in the histologic sections of liver tissues were the macrovesicular and microvesicular steatosis. Talpha(1) treatment protected the majority of the liver cells, while minimal macrovesicular and microvesicular steatosis was observed in the remaining cells. These results show that a high-fructose diet in rats leads to hepatic steatosis and a defect in the free radical defense system, and that treatment of Talpha(1) may improve these biochemical and morphologic changes in the fructose-fed rat livers.