Pharmaceutical biology · 2011
Antifibrotic effects of protocatechuic aldehyde on experimental liver fibrosis.
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Li Chunmei, Jiang Wanglin, Zhu Haibo, Hou Jian
Аннотация
BACKGROUND: Recent studies have demonstrated that transforming growth factor-β1 (TGF-β1) and connective transforming growth factor (CTGF) are associated with the pathophysiology of liver fibrosis. We isolated protocatechuic aldehyde, the major degradation of phenolic acids.
OBJECTIVE: This study was carried out to investigate the potential antifibrotic effect of Protocatechuic aldehyde (PA) on experimental liver fibrosis in vitro and in vivo, and to explore its possible mechanism.
MATERIALS AND METHODS: Cell proliferation was determined. Type I collagen, type III collagen, transforming growth factor-β1 (TGF-β1) and connective transforming growth factor (CTGF) were measured by ELISA kits in TNF-α stimulated HSCs. In the carbon tetrachloride (CCL(4))-induced rat liver fibrosis model, liver fibrosis grade and histopathological changes were evaluated, and biochemical indicators were determined. Furthermore, immunostaining and Western blot analysis were used to detect hepatic TGF-β1 and CTGF expression in liver tissue.
RESULTS: Overall, our results indicated that PA inhibits HSCs proliferation, inhibits the levels of TGF-β1, CTGF, type I collagen and type III collagen in TNF-α stimulated HSCs. Treatment of PA causes a significant reduction in fibrosis grade, ameliorates biochemical indicators and histopathological morphology, and reduces liver TGF-β1 and CTGF expression in rat model of CCL(4)-induced liver fibrosis.
CONCLUSION: These findings suggest that PA has potentially conferring antifibrogenic effects.
OBJECTIVE: This study was carried out to investigate the potential antifibrotic effect of Protocatechuic aldehyde (PA) on experimental liver fibrosis in vitro and in vivo, and to explore its possible mechanism.
MATERIALS AND METHODS: Cell proliferation was determined. Type I collagen, type III collagen, transforming growth factor-β1 (TGF-β1) and connective transforming growth factor (CTGF) were measured by ELISA kits in TNF-α stimulated HSCs. In the carbon tetrachloride (CCL(4))-induced rat liver fibrosis model, liver fibrosis grade and histopathological changes were evaluated, and biochemical indicators were determined. Furthermore, immunostaining and Western blot analysis were used to detect hepatic TGF-β1 and CTGF expression in liver tissue.
RESULTS: Overall, our results indicated that PA inhibits HSCs proliferation, inhibits the levels of TGF-β1, CTGF, type I collagen and type III collagen in TNF-α stimulated HSCs. Treatment of PA causes a significant reduction in fibrosis grade, ameliorates biochemical indicators and histopathological morphology, and reduces liver TGF-β1 and CTGF expression in rat model of CCL(4)-induced liver fibrosis.
CONCLUSION: These findings suggest that PA has potentially conferring antifibrogenic effects.
Предметные рубрики MeSH
AnimalsBenzaldehydesBlotting, WesternCarbon TetrachlorideCatecholsCell ProliferationCells, CulturedCollagen Type ICollagen Type IIIConnective Tissue Growth FactorCytoprotectionDisease Models, AnimalDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayHepatic Stellate CellsHyaluronic AcidImmunohistochemistryLamininLiverLiver CirrhosisMaleProtective AgentsRatsRats, Sprague-DawleyTransforming Growth Factor beta1Tumor Necrosis Factor-alpha