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Activation of peroxisome proliferator-activated receptor-gamma contributes to the inhibitory effects of curcumin on rat hepatic stellate cell growth.
Am J Physiol Gastrointest Liver Physiol. 2003 Jul; 285(1):G20-30.AJ

Abstract

Hepatic fibrogenesis occurs as a wound-healing process after many forms of chronic liver injury. Hepatic fibrosis ultimately leads to cirrhosis if not treated effectively. During liver injury, quiescent hepatic stellate cells (HSC), the most relevant cell type, become active and proliferative. Oxidative stress is a major and critical factor for HSC activation. Activation of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) inhibits the proliferation of nonadipocytes. The level of PPAR-gamma is dramatically diminished along with activation of HSC. Curcumin, the yellow pigment in curry, is a potent antioxidant. The aims of this study were to evaluate the effect of curcumin on HSC proliferation and to begin elucidating underlying mechanisms. It was hypothesized that curcumin might inhibit the proliferation of activated HSC by inducing PPAR-gamma gene expression and reviving PPAR-gamma activation. Our results indicated that curcumin significantly inhibited the proliferation of activated HSC and induced apoptosis in vitro. We demonstrated, for the first time, that curcumin dramatically induced the gene expression of PPAR-gamma and activated PPAR-gamma in activated HSC. Blocking its trans-activating activity by a PPAR-gamma antagonist markedly abrogated the effects of curcumin on inhibition of cell proliferation. Our results provide a novel insight into mechanisms underlying the inhibition of activated HSC growth by curcumin. The characteristics of curcumin, including antioxidant potential, reduction of activated HSC growth, and no adverse health effects, make it a potential antifibrotic candidate for prevention and treatment of hepatic fibrosis.

Authors+Show Affiliations

Dept. of Pathology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12660143

Citation

Xu, Jianye, et al. "Activation of Peroxisome Proliferator-activated Receptor-gamma Contributes to the Inhibitory Effects of Curcumin On Rat Hepatic Stellate Cell Growth." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 285, no. 1, 2003, pp. G20-30.
Xu J, Fu Y, Chen A. Activation of peroxisome proliferator-activated receptor-gamma contributes to the inhibitory effects of curcumin on rat hepatic stellate cell growth. Am J Physiol Gastrointest Liver Physiol. 2003;285(1):G20-30.
Xu, J., Fu, Y., & Chen, A. (2003). Activation of peroxisome proliferator-activated receptor-gamma contributes to the inhibitory effects of curcumin on rat hepatic stellate cell growth. American Journal of Physiology. Gastrointestinal and Liver Physiology, 285(1), G20-30.
Xu J, Fu Y, Chen A. Activation of Peroxisome Proliferator-activated Receptor-gamma Contributes to the Inhibitory Effects of Curcumin On Rat Hepatic Stellate Cell Growth. Am J Physiol Gastrointest Liver Physiol. 2003;285(1):G20-30. PubMed PMID: 12660143.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of peroxisome proliferator-activated receptor-gamma contributes to the inhibitory effects of curcumin on rat hepatic stellate cell growth. AU - Xu,Jianye, AU - Fu,Yumei, AU - Chen,Anping, Y1 - 2003/03/26/ PY - 2003/3/28/pubmed PY - 2003/7/25/medline PY - 2003/3/28/entrez SP - G20 EP - 30 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 285 IS - 1 N2 - Hepatic fibrogenesis occurs as a wound-healing process after many forms of chronic liver injury. Hepatic fibrosis ultimately leads to cirrhosis if not treated effectively. During liver injury, quiescent hepatic stellate cells (HSC), the most relevant cell type, become active and proliferative. Oxidative stress is a major and critical factor for HSC activation. Activation of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) inhibits the proliferation of nonadipocytes. The level of PPAR-gamma is dramatically diminished along with activation of HSC. Curcumin, the yellow pigment in curry, is a potent antioxidant. The aims of this study were to evaluate the effect of curcumin on HSC proliferation and to begin elucidating underlying mechanisms. It was hypothesized that curcumin might inhibit the proliferation of activated HSC by inducing PPAR-gamma gene expression and reviving PPAR-gamma activation. Our results indicated that curcumin significantly inhibited the proliferation of activated HSC and induced apoptosis in vitro. We demonstrated, for the first time, that curcumin dramatically induced the gene expression of PPAR-gamma and activated PPAR-gamma in activated HSC. Blocking its trans-activating activity by a PPAR-gamma antagonist markedly abrogated the effects of curcumin on inhibition of cell proliferation. Our results provide a novel insight into mechanisms underlying the inhibition of activated HSC growth by curcumin. The characteristics of curcumin, including antioxidant potential, reduction of activated HSC growth, and no adverse health effects, make it a potential antifibrotic candidate for prevention and treatment of hepatic fibrosis. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/12660143/Activation_of_peroxisome_proliferator_activated_receptor_gamma_contributes_to_the_inhibitory_effects_of_curcumin_on_rat_hepatic_stellate_cell_growth_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.00474.2002?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -