Department of Toxicology, College of Pharmacy, Chungnam National University, Daejeon 305-764, Republic of Korea.
Environ Toxicol Pharmacol. 2011 Jan;31(1):212-9. doi: 10.1016/j.etap.2010.10.011. Epub 2010 Nov 9.
During the process of liver fibrosis, hepatic stellate cells (HSCs) play a critical role in the increased formation and reduced degradation of extracellular matrix in the liver. We investigated the anti-proliferative effects of an anthocyanin fraction (AF), isolated from the purple-fleshed sweet potato, on platelet-derived growth factor (PDGF)-BB-dependent signaling pathways in HSC-T6 cells. HSC proliferation plays a pivotal role in liver fibrogenesis. The AF suppressed HSC activation, including PDGF-induced proliferation and α-smooth muscle actin (α-SMA) expression. Additionally, AF inhibited PDGF-BB-induced Akt and ERK1/2 phosphorylation. AF inhibited the phosphorylation level of PDGF receptor-β (PDGFR-β) following PDGF-BB stimulation, providing a mechanism for the inhibition of AF-mediated kinase. These results suggest that AF suppresses HSC proliferation by blocking PDGFR-β signaling, inhibiting Akt and ERK1/2 activation and α-SMA expression.
在肝纤维化过程中，肝星状细胞（HSCs）在肝脏中细胞外基质的增加形成和减少降解中起着关键作用。我们研究了从紫薯中分离的花色苷级分（AF）对血小板衍生生长因子（PDGF）-BB 依赖性信号通路在 HSC-T6 细胞中的抗增殖作用。HSC 增殖在肝纤维化发生中起着关键作用。AF 抑制 HSC 激活，包括 PDGF 诱导的增殖和α-平滑肌肌动蛋白（α-SMA）表达。此外，AF 抑制 PDGF-BB 诱导的 Akt 和 ERK1/2 磷酸化。AF 抑制 PDGF 受体-β（PDGFR-β）在 PDGF-BB 刺激后的磷酸化水平，为 AF 介导的激酶抑制提供了一种机制。这些结果表明，AF 通过阻断 PDGFR-β 信号、抑制 Akt 和 ERK1/2 激活以及α-SMA 表达来抑制 HSC 增殖。
