Relationship between oxidative stress levels and activation state on a hepatic stellate cell line

被引:45
作者
Guimaraes, ELM
Franceschi, MFS
Grivicich, I
Dal-pizzol, F
Moreira, JCF
Guaragna, RM
Borojevic, R
Margis, R
Guma, FCR
机构
[1] Univ Fed Rio Grande do Sul, ICBS, Dept Bioquim, BR-90035003 Porto Alegre, RS, Brazil
[2] Univ Luterana Brasil, Canoas, RS, Brazil
[3] Univ Fed Rio de Janeiro, Hosp Univ Clementino Fraga Filho, Dept Histol & Embriol, ICB, Rio de Janeiro, Brazil
[4] Univ Fed Rio de Janeiro, Hosp Univ Clementino Fraga Filho, PABCAM, Rio de Janeiro, Brazil
关键词
hepatic stellate cells; oxidative stress; activation state;
D O I
10.1111/j.1478-3231.2006.01245.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/Aims: Oxidative stress plays an important role in liver fibrosis. Under pathological conditions, hepatic stellate cells (HSC) undergo an activation process, developing a myofibroblast-like phenotype from the lipocyte phenotype. In this study, we determined the levels of oxidative stress and proliferation in different activation states of an experimental model of mouse HSC, the GRX cell line. These cells can be induced in vitro to display a more activated state or a quiescent phenotype. Methods/Results: We observed increased oxidative damage and higher levels of reactive oxygen species, measured by thiobarbituric acid reactive species and 2',7'-dichlorofluorescein diacetate, respectively, and diminished catalase activity in activated cells. Activation decreased proliferation and increased the number of cells in G2/M. Antioxidants N-acetylcysteine and Trolox varied in their capacity to correct the oxidative stress and proliferation status. Conclusion: The differences in physiological functions of stellate cell phenotypes suggest a relationship between oxidative stress levels and activation state.
引用
收藏
页码:477 / 485
页数:9
相关论文
共 47 条
[1]
Aldehydes potentiate α2(I) collagen gene activity by JNK in hepatic stellate cells [J].
Anania, FA ;
Womack, L ;
Jiang, MD ;
Saxena, NK .
FREE RADICAL BIOLOGY AND MEDICINE, 2001, 30 (08) :846-857
[2]
Overexpression of catalase in the mitochondrial or cytosolic compartment increases sensitivity of HepG2 cells to tumor necrosis factor-α-induced apoptosis [J].
Bai, JX ;
Cederbaum, AI .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (25) :19241-19249
[3]
Baroni GS, 1998, HEPATOLOGY, V27, P720
[4]
BEDOSSA P, 1994, HEPATOLOGY, V19, P1262, DOI 10.1016/0270-9139(94)90876-1
[5]
BOLOUKHERE M, 1993, J SUBMICR CYTOL PATH, V25, P505
[6]
BOROJEVIC R, 1985, IN VITRO CELL DEV B, V21, P382, DOI 10.1007/BF02623469
[7]
BOROJEVIC R, 1990, IN VITRO CELL DEV B, V26, P361
[8]
Intracellular signaling pathways in stellate cell activation [J].
Britton, RS ;
Bacon, BR .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1999, 23 (05) :922-925
[9]
Stages of activation of hepatic stellate cells: effects of ellagic acid, an inhibiter of liver fibrosis, on their differentiation in culture [J].
Buniatian, GH .
CELL PROLIFERATION, 2003, 36 (06) :307-319
[10]
DLPC decreases TGF-β1-induced collagen mRNA by inhibiting p38 MAPK in hepatic stellate cells [J].
Cao, Q ;
Mak, KM ;
Lieber, CS .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2002, 283 (05) :G1051-G1061