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  • Wu et al explored the anti inflammatory mechanisms


    Wu et al. explored the anti-inflammatory mechanisms by which osthole 35 acted on HepG2 cells cultured in a differentiated medium from cultured 3T3-L1 preadipocyte cells. HepG2 cells, a human liver cell line, were treated with various concentrations of osthole 35 in differentiated media from cultured 3T3-L1 cells to evaluate proinflammatory cytokines, inflammatory mediators, and signaling pathways. It was observed that Osthole 35 was able to suppress the levels of proinflammatory cytokines interleukin (IL)-1β and IL-6, as well as chemokines monocyte chemoattractant protein-1 and IL-8. In addition, COX-2 was suppressed and HO-1 expression was increased in a concentration-dependent manner. Osthole 35 also decreased IκB-α phosphorylation and suppressed the phosphorylation of MAPKs. Further it was observed osthole has anti-inflammatory effects as demonstrated by the decreased proinflammatory cytokine and mediator production through suppression of the NF-κB and MAPK signaling pathways in HepG2 cells when they are incubated on the differentiated medium Arctigenin from 3T3-L1 cells [65]. Furthermore, Li et al. reported pretreatment with osthole 35 restored the mRNA and protein levels of these factors, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) of ischemic penumbra cortices, suggesting that osthole possessed the function of preventing Arctigenin against ischemic damage [66]. Liao et al. studied osthole 35 from the seeds of Cnidium monnieri and demonstrated that osthole inhibited TNF-α, NO and COX-2 expression in LPS-stimulated macrophages, without reducing the expression of IL-6 [67]. Liu et al. studied inhibitory activity of the dichloromethane extract of the roots of Angelica pubescens f. biserrata on 5-lipoxygenase (5-LO) and cyclooxygenase (COX-1) in vitro. They observed prominent inhibitory effect of osthole and osthenol on 5-LO with IC50 values of 36.2 microM and 43.1 microM respectively [68]. The activity of Osthole 35 as Cox-2 inhibitors was further investigated by Wei et al. using a molecular modeling simulation which effectively showed that it has unique binding capabilities to both NOS and COX-2 [69]. Acute lung injury (ALI) is a life-threatening disease characterized by serious lung inflammation and increased capillary permeability. Isofraxidin (IF) 36, a Coumarin compound isolated from the natural medicinal plants such as Sarcandra glabra and Acanthopanax senticosus, which have been reported to have definite anti-bacterial, anti-oxidant, and anti-inflammatory activities. Niu et al. studied the protective effects and potential mechanism of IF against LPS-induced ALI in mice. IF inhibited lung histopathological changes and cyclooxygenase-2 (COX-2) protein expression. These results suggest that IF has a protective effect against LPS-induced ALI, and the protective effect of IF seems to result from the inhibition of COX-2 protein expression in the lung, which regulates the production of PGE2 [70]. Tong et al. reported isolation and inflammatory activity of prenylcoumarin omphalocarpin 37 from Radix Toddaliae Asiaticae, which has long been used as a traditional ethnic Chinese medicine for the treatment of inflammation and rheumatism. These results obtained in vitro and in vivo showed that the anti-inflammatory mechanism of omphalocarpin 37 might be attributed to the inhibition of pro-inflammatory mediators including nitric oxide, IL-6 and TNF-α. Omphalocarpin 37 decreased the overproduction of NO through down-regulation of the expression and enzymatic activity of iNOS and COX-2 in LPS-stimulated macrophage, which was due to the suppression of NF-κB activation in the transcriptional level. This is the first report of the anti-inflammatory activity of omphalocarpin 37 [71]. Wedelolactone (WEL) 38, a major coumestan ingredient in Wedelia chinensis, in traditional Chinese medicines were investigated by Yuan et al. for their anti-inflammatory effects and mechanism of WEL with a cellular model of lipopolysaccharide (LPS)-induced RAW 264.7 cells. It was observed that WEL (0.1, 1, 10μM) significantly inhibited the protein expression levels of iNOS and COX-2 in LPS-stimulated cells, as well as the downstream products, including NO, PGE2 and TNF-α. Furthermore, WEL also inhibited LPS-induced NF-κB p65 activation via the degradation and phosphorylation of IκB-α and subsequent translocation of the NF-κB p65 subunit to the nucleus, concluding the fact that WEL could be a potential for novel anti-inflammatory agent targeting on the NF-κB signaling pathways [72].