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Rosmarinic acid induces apoptosis of activated T cells from rheumatoid arthritis patients via mitochondrial pathway.

Hur, YG; Suh, CH; Kim, S; Won, J
Journal of clinical immunology, 27(1):36-45, 2007
Journal Title
Journal of clinical immunology
T cells play an important role in the initiation and the progression of rheumatoid arthritis (RA) and depletion of potentially pathogenic T cells was suggested as an important therapeutic protocol. We determined if rosmarinic acid (RosA), known as a secondary metabolite from herbal plants, had apoptotic activity toward T cells from RA patients and further verified target T-cell subsets. CD3(+)CD25(+) activated T-cell subsets from most of the RA patients displayed significantly higher apoptosis rates than did the PBMCs and total CD3(+) T cells. Furthermore, activated and effector CD4(+) T cells, including CD4(+)CD25(+) and CD4(+)CD45RO(+) T cells, had a tendency of being more susceptible to RosA-induced apoptosis than that of resting and naïve T-cell subsets. RosA induced the release of cytochrome c from mitochondria and the blockage of mitochondrial depolarization inhibited apoptosis. Taken together, these results suggest that RosA induces apoptosis of activated T-cell subsets from RA patients via a mitochondrial pathway.
MeSH terms
AdultAgedAntigens, CD3/immunologyApoptosis/drug effects*Apoptosis/immunologyArthritis, Rheumatoid/immunology*Cells, CulturedCinnamates/pharmacology*Cytochromes c/metabolismDepsides/pharmacology*FemaleHumansInterleukin-2 Receptor alpha Subunit/immunologyIntracellular Membranes/drug effectsIntracellular Membranes/immunologyLymphocyte Activation/immunology*MaleMembrane Potentials/drug effectsMembrane Potentials/immunologyMiddle AgedMitochondria/drug effectsT-Lymphocyte Subsets/cytologyT-Lymphocyte Subsets/drug effects*T-Lymphocyte Subsets/immunologyT-Lymphocytes, Regulatory/cytologyT-Lymphocytes, Regulatory/drug effectsT-Lymphocytes, Regulatory/immunology*
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Journal Papers > School of Medicine / Graduate School of Medicine > Rheumatology
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