Table 2.

Potential anti-RA mechanisms of some compounds.

Compound	Mechanism	Model	References
stigmasterol	Suppressed proinflammatory mediators and increased anti-inflammatory cytokine through down-regulating NF-kB, p65 and p38MAPK	CIA	Ahmad et al. (2020)30
β-Sitosterol	Inhibited synovial angiogenesis by suppressing endothelial cells proliferation and migration	CIA	Qian et al. (2022)31
	Repressed the M1 polarization and augmented M2 polarization	mø	Liu et al. (2019)48
Quercetin	Inhibited the release of proinflammatory cytokine (IL-6, TNF-α, IL-1β, IL-8, IL-13, IL-17) by activating SIRT1	CIA	Shen et al. (2021)49
	Inhibited NLRP3 inflammasome activation and activated HO-1-mediated anti-inflammatory response via modulating the Th17/Treg balance	CIA	Yang et al. (2017)50
	Inhibited IL-17 and RANKL production, suppressed Th17 cell	FLS	Kim et al. (2019)33
	Modulated the immune response to arthritis via attenuation of the purinergic system (E-NTPDase and E-ADA activities) and the levels of IFN-γ and IL-4	CFA	Saccol et al. (2019)51
Kaempferol	Inhibited RAFLS proliferation, migration, and inflammatory cytokines by suppressing FGFR3-RSK2 signaling	FLS	Lee et al. (2018)34
	Inhibited RAFLS migration and invasion by blocking MAPK pathway	FLS	Pan et al. (2017)52
	Enhanced the suppressive function of Treg cells by inhibiting FOXP3 phosphorylation	Treg	Lin et al. (2015)53
	Inhibited RAFLS proliferation, reduced MMPs, COX-2, and PGE2 production, inhibited NF-κB activation	FLS	Yoon et al. (2013)54