Capsaicin and sulforaphane prevent experimental liver fibrosis via upregulation of peroxisome proliferator-activated receptor gamma and nuclear factor (erythroid-derived 2)-like 2

Abstract

Capsaicin (CPS) and sulforaphane (SFN) have shown anti-carcinogenic, anti-inflammatory and antifibrogenic properties. The molecular mechanisms describing how these food compounds act remain unclear. This study was aimed at evaluating the molecular mechanisms of CPS and SFN on the hepatoprotective effect in a murine model. Animals were liver-injured via CCl4 intoxication and treated with CPS, SFN or both (CPS + SFN). In addition, we included a fibrosis control group (CCl4 + vehicle) and a healthy control group (vehicle only). Masson staining, qPCR, and Western blotting were performed in liver samples. AST and ALT determinations were performed in plasma. Our results showed less accumulation of overall extracellular matrix and downregulation of profibrogenic genes such as TGF-β1, COL1, TNF-α, and IL-6, in animals treated with CPS, SFN and CPS + SFN when compared with the fibrosis control group. Our findings suggest that this effect might be due to an increase of anti-inflammatory regulation by PPARγ and Nrf2-modulated antioxidant activity.

Keywords

• Capsaicin
• Sulforaphane
• PPARγ
• Nrf2
• Liver fibrosis