Format

Send to

Choose Destination
Front Biosci (Landmark Ed). 2020 Jan 1;25:498-512.

T-96 attenuates inflammation by inhibiting NF-κB in adjuvant-induced arthritis.

Author information

1
Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University; No.639 Longmian Avenue, Nanjing, 211198, P.R.China.
2
Laboratory Animal Center of Nanjing University of Chinese Medicine, Nanjing 210023, China.
3
Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University; No.639 Longmian Avenue, Nanjing, 211198, P.R.China, cl.xu81@gmail.com.

Abstract

The extract of the medicinal plant, Tripterygium wilfordii Hook. f. (TW), has been used in the treatment of diverse autoimmune diseases, including rheumatoid arthritis. However, the high frequency of toxic side effects has limited its clinical use. In order to reduce toxicity without losing the therapeutic benefit, the pharmacological activity and toxicity of four compounds (T-96, triptolide, neotripterifordin, and tripterifordin) from TW were evaluated. The current study revealed that these compounds interfere with the IL-1β signaling pathway, which stimulates the secretion of pro-inflammatory cytokines (IL-6) in primary rheumatoid arthritis synovial fibroblasts (RASFs). These compounds inhibit IL-6 production, and among these, T-96 was the most effective. Moreover, T-96 blocks activation of NF-kappa B and p38 and ameliorates the joint destruction and the clinical signs of the disease in adjuvant-induced arthritic rats. These data suggest that among the four compounds of the TW, T-96 possesses highest anti-rheumatoid arthritis activity though inhibiting IL-1-mediated inflammatory signaling pathways.

PMID:
31585899

Supplemental Content

Loading ...
Support Center