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.
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 ratliver 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.
Authors: Song Hee Lee; Bo Young Choi; A Ra Kho; Jeong Hyun Jeong; Dae Ki Hong; Sang Hwon Lee; Sang Yup Lee; Min Woo Lee; Hong Ki Song; Hui Chul Choi; Sang Won Suh Journal: Int J Mol Sci Date: 2018-01-08 Impact factor: 5.923
Authors: Sang Hwon Lee; Bo Young Choi; Song Hee Lee; A Ra Kho; Jeong Hyun Jeong; Dae Ki Hong; Sang Won Suh Journal: Int J Mol Sci Date: 2017-11-23 Impact factor: 5.923