Abstract
Pterocephalus hookeri was used as a traditional Chinese medicine for the treatment of rheumatoid arthritis. Sweroside was a main iridoid isolated from P. hookeri. The present study aimed to investigate the anti-inflammatory effect mechanism of sweroside. In RAW264.7 cells induced by lipopolysaccharide (LPS), the abnormal proliferation, the NO content increase, and the downregulated Sirtuin1 (SIRT1) expression were observed. Sweroside could alleviate the inflammation by inhibiting cell proliferation through arresting the cell cycle at the G0/G1 phase, by suppressing pro-inflammatory cytokines and by promoting anti-inflammatory cytokines in LPS-induced RAW264.7 cells. Further mechanism research indicated that sweroside could activate the SIRT1, then suppress the nuclear factor-kappa B (NF-κB) and promote the Forkhead transcription factor O1 (FOXO1) signaling pathways. The present study indicated that sweroside may be the main anti-inflammatory constituent of P. hookeri and a promising candidate for anti-inflammation therapy.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune disease which expresses as a symmetric polyarthritis associated with swelling and pain in multiple joints [1]
The results showed that the administration of NAM reversed the expressions of all proteins significantly, including SIRT1, NF-κB, N-NF-κB, FOXO1, N-FOXO1, i-nitric oxide synthases (NOSs), COX-2, IL-1β, IL-6, IL-10, tumor necrosis factor-α (TNF-α), MnSOD and P27, compared with the sweroside-treated groups (p < 0.05 or 0.01)
Our results indicated that LPS decreased the expression of SIRT1 in RAW264.7 cells, which was consistent with the previous report [19], suggesting the activation of SIRT1 might be a promising therapeutic strategy for inflammation
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune disease which expresses as a symmetric polyarthritis associated with swelling and pain in multiple joints [1]. RA significantly hampered the quality of people’s lives, covering 1% of the world’s population and leading to severe disability in the patients [2]. It was believed that inflammation have been involved in the development and progression of RA [3]. The inhibition of inflammation was an effective way to treat RA. Inflammation was a protective response of the immune system which would resist exogenous infection, recur the injury tissue and eliminate invading pathogens. Disordered inflammation might result in secondary damage and immune pathology, deteriorating diseases such as RA [4]. The development of effective anti-inflammatory drugs occupied the core position for the treatment of RA
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