Research articles
ScienceAsia 51 (2023): 1-11 |doi:
10.2306/scienceasia1513-1874.2023.008
Anti-inflammatory effect of Rhamnella gilgitica Mansf. et
Melch on complete Freund?s adjuvant induced-arthritis mice
and lipopolysaccharide (LPS)-treated RAW264.7 cells by
mediating the MAPK signaling pathway
Thubten Sambua,?, Tsering Dikyea,?, Tong Wangb, Liying Gaob, Bin Lib, Shan Huangb,*
ABSTRACT: Inflammation and oxidation are widely regarded as primary contributors to rheumatoid arthritis, with
macrophages such as murine RAW264.7 cells playing significant roles in the disease progression by secreting
inflammatory cytokines. Rhamnella gilgitica Mansf. et Melch (RG), a traditional Chinese plant medicine, has been shown
to have anti-inflammatory and anti-rheumatoid effects, although its underlying mechanism remains unclear. In this
study, we confirmed the anti-inflammatory and anti-oxidative effects of RG and investigated its protective mechanism.
The active components of RG were analyzed using LC-MS/MS. The components found included ursolic acid, daidzin,
simvastatin, chlorogenic acid, casticin, kaempferol, naringenin, azelanic acid, and vanillic acid. In addition, the contents
of kaempferol and naringenin were examined by HPLC. Results showed that RG significantly improved ankle joint
swelling, arthritis index, paw thickness, and ankle joint thickness; with decreasing serum levels of pro-inflammatory
cytokines? such as IL-1?, IL-6, TNF-?, and RF. Furthermore, RG also inhibited the protein expression levels of IL-10
and IL-17, as well as the protein phosphorylation of MAPK signaling pathway including JNK, ERK, and P38 in ankle
cartilage of mice. In vivo, RG decreased the levels of NO, IL-1?, IL-6, TNF-?. and IL-17. Additionally, RG inhibited the
protein phosphorylation of JNK, ERK, and P38 in RAW264.7 cells stimulated by LPS. Overall, results suggested that
the underlying anti-inflammatory effects of RG could be associated with the inhibition of JNK, ERK, and P38 protein
phosphorylation.
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| a |
The department of Tibetan Medicine, University of Tibetan Medicine, Lhasa 850000 China |
| b |
Department of Pharmacy, Key Laboratory of Pharmaceutical Research for Metabolic Diseases,
Qingdao University of Science & Technology, Qingdao 266042 China |
* Corresponding author, E-mail: huangshan@qust.edu.cn
Received 27 May 2023, Accepted 29 Nov 2024
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