Effect of exogenous interleukin-10 on carbon tetrachloride CCL4-induced hepatic fibrosis in rats

الملخص EN

Background : Transforming growth factor β1 (TGF-β1) is one of the strongest profibrotic cytokines and TGF-β1 / Smad signaling is the cardinal signal transduction pathway involved in fibrosis.

Previ-ous studies indicated that exogenous IL-10 down regulates collagen type I.

It also exerts antifibrogenic effect by down regulating profibrogenic cytokines such as (TGF-β1).

All these stud-ies indicate that IL-10 might become a new therapeutic target.

Aim : To investigate the potential therapeutic effect of exogenous interleukin-10 on reversing the well-established hepatic fibrosis of CCl4 administration in experimental rats.

Materials and Methods : Albino rats were divided into four groups (27 rats each) : group A (control), group B1 (CCl4-treated), group B2 (spontaneous re-covery, SR) and group B3 (IL-10-treated).

Rats' liver tissue was stained with i) hematoxylin and eosin (H & E) and, ii) Masson’s trichrome stains for evaluation of the histological activity index (HAI).

Serum TGF-β1 was determined by ELISA.

Results : No inflammation was found in the control group, however, marked inflammation (grade 3) was observed in CCl4-induced fibrosis group while moderate inflammation (grade 2) was observed in SR group.

Meanwhile the administration of IL-10 in group D resulted in a marked decrease in the grading of inflammation (grade 1) com-pared to CCl4-induced fibrosis group.

No fibrosis was observed in the control group, however, a marked fibrosis reaching to cirrhosis (stages 3&4) was observed in CCl4-induced fibrosis group.

The degree of fibrosis showed a mild decrease (stage 3) in SR group.

Meanwhile the administra-tion of IL-10 in group D resulted in a marked decrease in the stage of fibrosis to (stage 1).

Serum TGF-β1 concentration dramatically increased in CCl4-induced fibrosis group compared to the con-trol group.

It also increased in SR group, but lesser than CCl4 treated group while it was signifi-cantly reduced in the IL-10 treated group.

Conclusions : Our results provide evidence towards the potential effect of IL-10 as anti-TGF-β1 that could lead to a reduction of hepatic fibrosis.