Oncotarget

Research Papers:

Ginsenoside Rg1 attenuates adjuvant-induced arthritis in rats via modulation of PPAR-γ/NF-κB signal pathway

Leiming Zhang _, Maojing Zhu, Minmin Li, Yuan Du, Sijin Duan, Yanan Huang, Yongying Lu, Jianqiao Zhang, Tian Wang and Fenghua Fu

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Oncotarget. 2017; 8:55384-55393. https://doi.org/10.18632/oncotarget.19526

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Abstract

Leiming Zhang1,*, Maojing Zhu1,*, Minmin Li1,*, Yuan Du1, Sijin Duan1, Yanan Huang1, Yongying Lu1, Jianqiao Zhang1, Tian Wang1 and Fenghua Fu1

1School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, P.R. China

*These authors contributed equally to this work

Correspondence to:

Leiming Zhang, email: [email protected]

Fenghua Fu, email: [email protected]

Keywords: ginsenoside Rg1, adjuvant-induced arthritis, PPAR-γ, IκBα, NF-κB

Received: May 24, 2017     Accepted: July 13, 2017     Published: July 24, 2017

ABSTRACT

Ginsenoside Rg1, the main active compound in Panax ginseng, has already been shown to have anti-inflammatory effects. However, the protective effects of Rg1 on rheumatoid arthritis (RA) remain unclear. The aim of the present study was to investigate the effects and mechanisms of Rg1 on adjuvant-induced arthritis (AIA) in rats. AIA rats were given Rg1 at doses of 5, 10, and 20 mg/kg intraperitoneally for 14 days to observe the anti-arthritic effects. The results showed that Rg1 significantly alleviated joint swelling and injuries. Rg1 can also significantly reduce the level of TNF-α and IL-6, increase PPAR-γ protein expression, inhibit IκBα phosphorylation and NF-κB nuclear translocation in the inflammatory joints of AIA rats and RAW264.7 cells stimulated by lipopolysaccharide (LPS). The results indicate that Rg1 has therapeutic effects on AIA rats, and the mechanism might be associated with its anti-inflammatory effects by up-regulating PPAR-γ and subsequent inhibition of NF-κB signal pathway.


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