Abstract Title:

Astragaloside IV suppresses inflammatory mediator production in synoviocytes and collagen‑induced arthritic rats.

Abstract Source:

Mol Med Rep. 2016 Apr ;13(4):3289-96. Epub 2016 Feb 22. PMID: 26936538

Abstract Author(s):

Hao Xu, Chang-Yao Wang, Hai-Ning Zhang, Cheng-Yu Lv, Ying-Zhen Wang

Article Affiliation:

Hao Xu


The aim of the current study was to investigate the effects of Astragaloside‑IV (AS‑IV) on inflammatory mediators in synoviocytes and collagen‑induced arthritic rats. Synoviocytes were stimulated with lipopolysaccharides (LPS) and Sprague‑Dawley rats were injected with type II collagen. AS‑IV was administered to the LPS‑stimulated synoviocytes and collagen‑induced arthritis (CIA) rats. The inflammation of LPS‑stimulated synoviocytes and CIA rats was assessed using enzyme‑linked immunosorbent assays and western blotting. Using Cell Counting Kit‑8 analysis, it was demonstrated that AS‑IV (5, 20 and 50 mg/ml) inhibited the LPS‑stimulated synoviocytes proliferation in a dose‑dependent manner. AS‑IV significantly inhibited the LPS‑stimulated inflammatory response, as indicated by the expression levels of TNF‑α, IL‑1β, IL‑6 and IL‑8. In addition, treatment with AS‑IV significantly reduced the LPS‑stimulated cyclooxygenase (COX)‑1, COX‑2, high mobility group box 1 protein (HMGB1) and intercellular adhesion molecule 1 overexpression, and intranuclear nuclear factor (NF)‑κBp65 subunit accumulation and activation of c‑Jun N‑terminal kinase (JNK)1/2 and p38. Similar to the protective effects of AS‑IV on LPS‑stimulated synoviocytes, AS‑IV treatment significantly reduced the expression levels of tumor necrosis factor α, interleukin (IL)‑1β, IL‑6 and IL‑8 expression levels, and attenuated intranuclear NF‑κBp65 subunit accumulation and overexpression of COX‑2 and inducible nitric oxide synthase in CIA rats. In conclusion, the results of the present study demonstrated for the first time, to the best of our knowledge, that AS‑IV protects synoviocytes against LPS‑ and collagen‑induced inflammatory responses through inhibition of the HMGB1‑dependent JNK1/2‑ and p38‑activated NF‑κB/COX‑2 pathway.

Print Options

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2021 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.