IMR Press / FBL / Volume 25 / Issue 3 / DOI: 10.2741/4816

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

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

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1 Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China
2 Laboratory Animal Center of Nanjing University of Chinese Medicine, Nanjing 210023, China
3 Jiangsu Center for Pharmacodynamics Research and Evaluation, China Pharmaceutical University, Nanjing 210009, China
4 Key Laboratory of Drug Quality Control and Pharmacovigilance, China Pharmaceutical University, Ministry of Education, Nanjing 210009, China
5 Center for Drug Screening and Pharmacodynamics Evaluation, School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China
Front. Biosci. (Landmark Ed) 2020, 25(3), 498–512; https://doi.org/10.2741/4816
Published: 1 January 2020
(This article belongs to the Special Issue Leader sequences of coronavirus are altered during infection)
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-κB 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.

Keywords
T-96
NF-kappaB
Rheumatoid Arthritis
Fibroblast-like synoviocytes
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