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Triptolide (PG-490) induces apoptosis of dendritic cells through sequential p38 MAP kinase phosphorylation and caspase 3 activation.

Authors
  • Liu, Qiuyan
  • Chen, Taoyong
  • Chen, Huabiao
  • Zhang, Minghui
  • Li, Nan
  • Lu, Zhanjun
  • Ma, Pengcheng
  • Cao, Xuetao
Type
Published Article
Journal
Biochemical and biophysical research communications
Publication Date
Jul 02, 2004
Volume
319
Issue
3
Pages
980–986
Identifiers
PMID: 15184078
Source
Medline
License
Unknown

Abstract

Dendritic cells (DCs) are the most potent antigen-presenting cells that play crucial roles in the regulation of immune response. Triptolide, an active component purified from the medicinal plant Tripterygium wilfordii Hook F., has been demonstrated to act as a potent immunosuppressive drug capable of inhibiting T cell activation and proliferation. However, little is known about the effects of triptolide on DCs. The present study shows that triptolide does not affect phenotypic differentiation and LPS-induced maturation of murine DCs. But triptolide can dramatically reduce cell recovery by inducing apoptosis of DCs at concentration as low as 10ng/ml, as demonstrated by phosphatidylserine exposure, mitochondria potential decrease, and nuclear DNA condensation. Triptolide induces activation of p38 in DCs, which precedes the activation of caspase 3. SB203580, a specific kinase inhibitor for p38, can block the activation of caspase 3 and inhibit the resultant apoptosis of DCs. Our results suggest that the anti-inflammatory and immunosuppressive activities of triptolide may be due, in part, to its apoptosis-inducing effects on DCs.

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