Differential Inhibitory Effects of Salvianolic Acids on Activation of Rat Hepatic Stellate Cells by Platelet-Derived Growth Factor

被引：15

作者：

Tsai, Ming-Kuei ^{[2
]}

Lin, Yun-Lian ^{[1
]}

Huang, Yi-Tsau ^{[2
]}

机构：

[1] Natl Res Inst Chinese Med, Div Med Chem, Taipei 112, Taiwan

[2] Natl Yang Ming Univ, Inst Tradit Med, Taipei 112, Taiwan

来源：

PLANTA MEDICA | 2011年 / 77卷 / 13期

关键词：

hepatic stellate cells; salvianolic acid; platelet-derived growth factor; oxidative stress; hepatic fibrosis; Salvia miltiorrhiza; Lamiaceae; PROTEIN-KINASE-C; SMOOTH-MUSCLE-CELLS; NF-KAPPA-B; NADPH-OXIDASE; INCREASED PROLIFERATION; OXIDATIVE STRESS; SURVIVAL; THIOREDOXIN; PHOSPHORYLATION; DIACYLGLYCEROL;

D O I：

10.1055/s-0030-1270783

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

Platelet-derived growth factor (PDGF) induces cell proliferation together with oxidative stress. The present study investigated the effects of salvianolic acid A (Sal A) and B (Sal B) on the PDGF-induced signaling cascades in hepatic stellate cells (HSCs). HSC-T6, a rat hepatic stellate cell line, was stimulated with PDGF (10 ng/mL). The inhibitory effects of Sal A and B on oxidative stress-related signaling pathways were assessed in vitro. The protein levels were measured by Western blotting. FACS analysis was applied to detect the thioredoxin (Trx) level. Sal A and B showed different inhibitory abilities on the PDGF-related pathway. Sal A inhibited 70-kDa ribosomal S6 kinase (p70(s6k)) and associated proteins. Sal B attenuated PDGF-induced c-jun-N-terminal kinase (JNK), p38, and PKC-delta phosphorylations. Both Sal A and B diminished the activation of PKD, Trx, hemeoxygenase (HO)-1, and Nrf2. Taken together, our results showed that Sal A and B attenuated PDGF-induced ROS formation in HSCs, possibly through different signaling pathways.

引用

页码：1495 / 1503

页数：9

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