Amelioration of Hepatotoxicity by Sodium Butyrate Administration in Rats

Abstract

Lead poisoning is a serious environmental issue with life-threatening consequences. Lead poisoning increases the risk of cancers, gastrointestinal disorders, hepatotoxicity, central nervous system diseases, nephropathy, and cardiovascular diseases in animals and humans. The current study aimed to investigate the effect of sodium butyrate, as an antioxidant, on protecting female adult rats from the harmful effects of lead acetate. A total of 40 adult female albino rats were divided randomly into four equal groups. The first group dealt as the control. The second group received lead acetate at a dose of 200 mg/kg daily orally. The third group received lead acetate at a dose of 50 mg/kg daily orally, and the fourth group received both sodium butyrate and lead acetate orally/day for 35 days. The result indicated that sodium butyrate reduced the concentration of liver enzymes (ALT, AST, and ALP) which were elevated by lead acetate poising. Moreover, sodium butyrate ameliorates the redux status by decreasing malondialdehyde and increasing total antioxidant capacity. Additionally, sodium butyrate-treated rats showed significant alterations in the expression of peroxisome proliferator-activated receptor gamma and interleukin -10 genes. In conclusion, this study reveals an unrecognized role for peroxisome proliferator-activated receptor gamma and Interleukin-10 signaling after sodium butyrate treatment in regulating the immunopathology that occurs during lead acetate poising.