Asset Details
Do you wish to reserve the book?
A two-herb formula inhibits hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
A two-herb formula inhibits hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes
Do you wish to request the book?
A two-herb formula inhibits hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
A two-herb formula inhibits hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes
2021
Overview
Fibroblast-like synoviocytes (FLS) play a pathogenic role in rheumatoid arthritis (RA). STAT3 signaling is activated in FLS of RA patients (RA-FLS), which in turn causes RA-FLS hyperproliferation. RL is a traditional remedy for treating inflammatory diseases in China. It comprises Rosae Multiflorae Fructus and Lonicerae Japonicae Flos. A standardized ethanolic extract of RL (RLE) has been shown to exert anti-arthritic effects in collagen-induced arthritis (CIA) rats. Some constituents of RLE were reported to inhibit JAK2/STAT3 signaling in rat FLS. Here, we determined whether RLE inhibits FLS hyperproliferation, and explored the involvement of STAT3 signaling in this inhibition. In joints of CIA rats, RLE increased apoptotic FLS. In IL-6/sIL-6R-stimulated RA-FLS, RLE reduced cell viability and evoked cell apoptosis. In synovial tissues of CIA rats, RLE lowered the protein level of phospho-STAT3. In IL-6/sIL-6R-stimulated RA-FLS, RLE inhibited activation/phosphorylation of STAT3 and JAK2, decreased the nuclear localization of STAT3, and downregulated protein levels of Bcl-2 and Mcl-1. Over-activation of STAT3 diminished RLE’s anti-proliferative effects in IL-6/sIL-6R-stimulated RA-FLS. In summary, RLE inhibits hyperproliferation of FLS in rat and cell models, and suppression of STAT3 signaling contributes to the underlying mechanisms. This study provides further pharmacological groundwork for developing RLE as a modern anti-arthritic drug.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 692/4023
/ Animals
/ Arthritis, Rheumatoid - drug therapy
/ Arthritis, Rheumatoid - metabolism
/ Collagen
/ Drug Evaluation, Preclinical
/ Drugs, Chinese Herbal - pharmacology
/ Drugs, Chinese Herbal - therapeutic use
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Lonicera
/ Plant Extracts - therapeutic use
/ Rats
/ Rosa
/ Science
