Dandelion polysaccharide treatment protects against dextran sodium sulfate-induced colitis by suppressing NF-κB/NLRP3 inflammasome-mediated inflammation and activating Nrf2 in mouse colon.

The treatment of ulcerative colitis (UC) is still an intractable medical problem. Polysaccharides are promising candidates for the treatment of UC and have received widespread attention in recent years. The objective of this study was to explore the protective effect and underlying mechanism of dandelion polysaccharide (DP) on dextran sulfate sodium (DSS)-induced colitis in mice. Our results showed that oral administration of DP could dramatically alleviate colonic lesions, as evidenced by reduced DAI scores, shortening of colon length, and ameliorating pathologic abnormalities in colons. Additionally, the expressions of pro-inflammatory factors (TNF-α, IL-1ß, and IL-6) and the infiltration of inflammation-regulation cells, marked by myeloperoxidase and F4/80, were also inhibited after DP treatment. Moreover, DP treatment also markedly suppressed the nuclear translocation of NF-κB-p65 and the activation of the NLRP3 inflammasome. Furthermore, DP also activated the Nrf2/HO-1 pathway and reduced the oxidative stress induced by DSS. Overall, these results suggest that DP could be a promising novel therapeutic approach for the treatment of UC.

Allyl methyl trisulfide protected against LPS-induced acute lung injury in mice via inhibition of the NF-κB and MAPK pathways.

Allyl methyl trisulfide (AMTS) is one major lipid-soluble organosulfur compound of garlic. Previous studies have reported the potential therapeutic effect of garlic on acute lung injury (ALI) or its severe condition acute respiratory distress syndrome (ARDS), but the specific substances that exert the regulatory effects are still unclear. In this study, we investigate the protective effects of AMTS on lipopolysaccharide (LPS)-induced ALI mice and explored the underlying mechanisms. In vivo experiments, ICR mice were pretreated with 25-100 mg/kg AMTS for 7 days and followed by intratracheal instillation of LPS (1.5 mg/kg). The results showed that AMTS significantly attenuated LPS-induced deterioration of lung pathology, demonstrated by ameliorative edema and protein leakage, and improved pulmonary histopathological morphology. Meanwhile, the expression of inflammatory mediators and the infiltration of inflammation-regulation cells induced by LPS were also inhibited. In vitro experiments also revealed that AMTS could alleviate inflammation response and inhibit the exaggeration of macrophage M1 polarization in LPS-induced RAW264.7 cells. Mechanistically, we identified that AMTS treatment could attenuate the LPS-induced elevation of protein expression of p-IκBα, nuclear NF-κB-p65, COX2, iNOS, p-P38, p-ERK1/2, and p-JNK. Collectively, these data suggest that AMTS could attenuate LPS-induced ALI and the molecular mechanisms should be related to the suppression of the NF-κB and MAPKs pathways.