Bi Siling, Chu Fuhao, Wang Mina, Li Bi, Mao Pei, Zhang Huazheng, Wang Penglong, Guo Wenbo, Xu Liang, Ren Liwei, Lei Haimin, Zhang Yuzhong
Department of Pathology, Beijing University of Chinese Medicine, Beijing 100102, China.
School of Chinese Pharmacy, Beijing University of Chinese Medicine, Beijing 100102, China.
Molecules. 2016 Nov 23;21(11):1599. doi: 10.3390/molecules21111599.
Hepatic fibrosis is a naturally occurring wound-healing reaction, with an imbalance of extracellular matrix (ECM) during tissue repair response, which can further deteriorate to hepatocellular carcinoma without timely treatment. Inhibiting activated hepatic stellate cell (HSC) proliferation and inducing apoptosis are the main methods for the treatment of liver fibrosis. In our previous study, we found that the TOA-glycine derivative (G-TOA) had exhibited more significant inhibitory activity against HepG2 cells and better hydrophilicity than TOA, ligustrazine (TMP), and oleanolic acid (OA). However, inhibiting activated HSC proliferation and inducing apoptosis by G-TOA had not been reported. In this paper, the selective cytotoxicity of G-TOA was evaluated on HSC-T6 cells and L02 cells, and apoptosis mechanisms were explored. It was found that G-TOA could selectively inhibit the proliferation of activated HSC-T6 cells, induce morphological changes, early apoptosis, and mitochondrial membrane potential depolarization, increase intracellular free calcium levels, downregulate the expression of NF-κB/p65 and COX-2 protein, and decrease the ratio of Bcl-2/Bax, thereby inducing HSC-T6 cell apoptosis. Thence, G-TOA might be a potential antifibrosis agent for the therapy of hepatic fibrosis, provided that it exerts anti-fibrosis effects on activated HSC-T6 cells.
肝纤维化是一种自然发生的伤口愈合反应,在组织修复反应过程中细胞外基质(ECM)失衡,若不及时治疗可进一步恶化为肝细胞癌。抑制活化的肝星状细胞(HSC)增殖并诱导其凋亡是治疗肝纤维化的主要方法。在我们之前的研究中,我们发现TOA-甘氨酸衍生物(G-TOA)对HepG2细胞表现出比TOA、川芎嗪(TMP)和齐墩果酸(OA)更显著的抑制活性以及更好的亲水性。然而,尚未有关于G-TOA抑制活化HSC增殖并诱导其凋亡的报道。本文评估了G-TOA对HSC-T6细胞和L02细胞的选择性细胞毒性,并探讨了其凋亡机制。研究发现,G-TOA可选择性抑制活化的HSC-T6细胞增殖,诱导细胞形态变化、早期凋亡和线粒体膜电位去极化,增加细胞内游离钙水平,下调NF-κB/p65和COX-2蛋白的表达,并降低Bcl-2/Bax比值,从而诱导HSC-T6细胞凋亡。因此,倘若G-TOA对活化的HSC-T6细胞发挥抗纤维化作用,它可能是一种治疗肝纤维化的潜在抗纤维化药物。