Anti-inflammatory, anti-oxidant and hepatoprotective effects of lactoferrin in rats

Carbon tetrachloride (CCl₄) is a strong hepatotoxic agent. The ability of the anti-inflammatory agent, lactoferrin (LF), to alleviate hepatic inflammation in a Wistar rat model administered with carbon tetrachloride (CCl₄) was examined. Thirty male Wistar rats were segregated into 5 groups (6 rats per group): Control group, LF group (300 mg LF/kg b. wt daily for three weeks), CCl₄ group (1 ml CCl₄/kg b. wt once orally), LF-protected group (300 mg LF/kg b. wt daily for 3 weeks followed by 1 mL CCl₄/kg b. wt once orally), and LF-treated group (1 mL CCl₄/kg b.wt once orally followed by 300 mg LF/kg b. wt orally every day for three weeks). Erythrogram, leukogram, activity of oxidative stress markers (Superoxide dismutase [SOD], Glutathione peroxidase [GPx], and Malondialdehyde [MDA]), and expression of hepatic paraoxonase-1 (PON1), interleukin (IL)-1β, and IL-10 mRNA were determined. Histopathological examination of the hepatic tissue was carried out. CCl₄ caused liver injury, loss of liver antioxidant activity of SOD and GPx, and a significant increase in the level of malondialdehyde in the serum. Moreover, CCl₄ induced up-regulation of hepatic pro-inflammatory (IL-1β) factors, and down-regulation of anti-inflammatory (IL-10 and PON1) factors. Based on histopathological examination, the hepatic tissues had severe inflammation and were damaged. However, LF mitigated the liver damage, oxidative stress, and hepatotoxicity caused by CCl₄. Overall, these results suggest that LF-mediated immunological mechanisms alleviate CCl4-induced hepatic toxicity and provide a novel perspective on the potential use of LF for prophylactic and therapeutic applications in treating liver diseases.