Authors : Wael Nasr El-Din, Gamal Hassan, Alaa El-Din Abdel-Hamed, Amr Kamel
DOI : 10.21608/scumj.2013.45657
Volume : 16
Issue : 1
Year : 2013
Page No : 29-36
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. Previous 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 studies 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 recovery, S R) 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 administrationof 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 administration 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 control group. It also increased in SR group, but lesser than CCl4 treated group while it was significantly 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.