Zvibel Isabel, Bar-Zohar Dan, Kloog Yoel, Oren Ran, Reif Shimon
Gastroenterology Institute, Tel Aviv Sourasky Medical Center, Weizmann 6, Tel Aviv, Israel.
Dig Dis Sci. 2008 Apr;53(4):1048-53. doi: 10.1007/s10620-007-9984-0. Epub 2007 Oct 13.
In vivo inhibition of Ras by its antagonist farnesylthiosalicylic acid (FTS) prevents and reverses liver fibrosis in a rat model. In this study we showed the in vitro effects of Ras inhibition in a rat hepatic stellate cell line, HSC-T6. The IC(50) of FTS that inhibited PDGF-induced proliferation was 15 microM. FTS, by itself or in combination with PDGF, induced a three- to fivefold increase in the number of apoptotic stellate cells but did not induce apoptosis in cells cultured with TGFbeta1. We observed increased activity of MMP-9 and MMP-2 induced by FTS in combination with PDGF or TGFbeta. FTS, alone or in the presence of PDGF and TGFbeta, reduced collagen I mRNA expression. In conclusion, the in vivo amelioration of liver fibrosis by FTS may be explained by its ability to inhibit hepatic stellate cell proliferation, induce apoptosis and MMP-2 and MMP-9 activity, and decrease collagen I expression.
在大鼠模型中,其拮抗剂法尼基硫代水杨酸(FTS)对Ras的体内抑制作用可预防和逆转肝纤维化。在本研究中,我们展示了Ras抑制在大鼠肝星状细胞系HSC-T6中的体外效应。抑制血小板衍生生长因子(PDGF)诱导的增殖的FTS的半数抑制浓度(IC50)为15微摩尔。FTS单独或与PDGF联合使用,可使凋亡星状细胞数量增加三至五倍,但在用转化生长因子β1(TGFβ1)培养的细胞中不诱导凋亡。我们观察到FTS与PDGF或TGFβ联合诱导的基质金属蛋白酶-9(MMP-9)和基质金属蛋白酶-2(MMP-2)活性增加。FTS单独或在存在PDGF和TGFβ的情况下,均可降低I型胶原mRNA表达。总之,FTS对肝纤维化的体内改善作用可能归因于其抑制肝星状细胞增殖、诱导凋亡以及MMP-2和MMP-9活性并降低I型胶原表达的能力。