Astilbin from Smilax glabra Roxb. Attenuates Inflammatory Responses in Complete Freund’s Adjuvant-Induced Arthritis Rats

Figure 6

Schematic diagram of alleviation of rheumatoid arthritis (RA) by astilbin (GZ-SGR). The canonical pathway NF-κB is involved in the pathogenesis of RA. In the cytoplasm, NF-κB proteins are usually associated with inhibitors of NF-κB (IκBs). External stimuli, including ligation of receptors of proinflammatory cytokines, activate the TLR adaptor MyD88 and subsequently stimulate the IκB kinase (IKK) molecules, including IKKβ. IKK phosphorylates IκBs, leading to their degradation, thereby allowing NF-κB to enter the nucleus and activate genes that contribute to chronic inflammation, such as cytokines, chemokines, and tumor necrosis factor receptors (TNFR). Astilbin, isolated from GZ-SGR, can reduce proinflammatory cytokines production, including TNF-α, IL-1β, and IL-6, and decrease the protein expression of MyD88, IKKβ, and p65, the key components that play important roles in TLRs-NF-κB pathway in RA development.