Universidad de Murcia. Departamento de Biología Celular e Histología
Abstract
Liver fibrosis is an excessive accumulation
of scar tissue resulting from inflammation and cell death.
Thioacetamide (TAA) is a well-known hepatotoxin that
induces liver fibrosis. A marker of injured hepatocytes is
transforming growth factor-beta 1 (TGF-β1), while
alpha-smooth muscle actin (α-SMA) and tissue inhibitor
of metalloproteinase 1 (TIMP-1) are markers of
activated hepatic stellate cells. Alpha-mangostin, a major
xanthone derivative from the mangosteen pericarp, has
been shown to have anti-oxidant and anti-inflammatory
activities. The objective of this study was to determine
whether alpha-mangostin has a protective effect on
TAA-induced liver fibrosis in rats. The rats were treated
by intraperitoneal injection of compounds for eight
weeks. For the control group a mixture of dimethyl
sulfoxide and phosphate buffered saline was
administered. Two hundred mg/kg BW of TAA was
administered three times weekly. Alpha-mangostin was
administered at 5 mg/kg BW and silymarin at 100 mg/kg
BW, both twice weekly. TAA induced histologically
recognizable liver damage and fibrosis, as anticipated.
Furthermore, it increased immunohistochemically
detectable TGF-β1, α-SMA, and TIMP-1. Coadministration of alpha-mangostin or silymarin with
TAA prevented or ameliorated the effects of TAA
administration alone. The anti-fibrotic effect of alphamangostin was stronger than that of silymarin