RESEARCH - Curcumin induces apoptosis and inhibits prostaglandin E(2) production in synovial fibroblasts of patients with RA

[Guest guest]

Int J Mol Med. 2007 Sep;20(3):365-72.

Curcumin induces apoptosis and inhibits prostaglandin E(2) production

in synovial fibroblasts of patients with rheumatoid arthritis.

Park C, Moon DO, Choi IW, Choi BT, Nam TJ, Rhu CH, Kwon TK, Lee WH,

Kim GY, Choi YH.

Department of Biochemistry, Dongeui University College of Oriental

Medicine, Busan 614-052, Korea.

Rheumatoid arthritis (RA) is a chronic inflammatory disease that is

characterized by hyperplasia of the synovial fibroblasts, which is

partly the result of decreased apoptosis. This study investigated the

mechanisms through which curcumin, a polyphenolic compound from the

rhizome of Curcuma longa, exerts its anti-proliferative action in the

synovial fibroblasts obtained from patients with RA. Exposure of the

synovial fibroblasts to curcumin resulted in growth inhibition and the

induction of apoptosis, as measured by MTT assay, fluorescent

microscopy and Annexin-V-based assay. RT-PCR and immunoblotting showed

that treating the cells with curcumin resulted in the down-regulation

of anti-apoptotic Bcl-2 and the X-linked inhibitor of the apoptosis

protein as well as the up-regulation of pro-apoptotic Bax expression

in a concentration-dependent manner. Curcumin-induced apoptosis was

also associated with the proteolytic activation of caspase-3 and

caspase-9, and the concomitant degradation of poly(ADP-ribose)

polymerase protein. Furthermore, curcumin decreased the expression

levels of the cyclooxygenase (COX)-2 mRNA and protein without causing

significant changes in the COX-1 levels, which was correlated with the

inhibition of prostaglandin E(2) synthesis. These results show that

curcumin might help identify a new therapeutic pathway against

hyperplasia of the synovial fibroblasts in RA.

PMID: 17671742

http://www.ncbi.nlm.nih.gov/pubmed/17671742

Not an MD