The anti-inflammatory effects of baicalin through suppression of NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes

摘要

In this study, the anti-inflammatory effects and mechanisms of baicalin on LPS-induced NLRP3 inflammatory pathway were investigated in piglet mononuclear phagocytes (control, LPS stimulation, LPS stimulation+12.5 mu g/ml baicalin, LPS stimulation+25 mu g/ml baicalin, LPS stimulation+50 mu g/ml baicalin and LPS stimulation+100 mu g/ml baicalin). The levels of reactive oxygen species (ROS), the secretion levels of IL-1, IL-18 and TNF-, mRNA expression levels of IL-1, IL-18, TNF- and NLRP3, as well as the protein levels of cleaved caspase-1 p20 were significantly increased after LPS-challenge invitro. However, LPS stimulation did not influence apoptosis-associated speck-like protein and caspase-1 mRNA levels, which are also components of the NLRP3 inflammasome. Baicalin at 50 mu g/ml and 100 mu g/ml could inhibit the production of ROS, TNF-, IL-1 and IL-18, and down-regulate mRNA expression of IL-1, IL-18, TNF- and NLRP3, as well as expression of cleaved caspase-1 p20. These results showed that the anti-inflammatory effects of baicalin occurred via the regulation of the release of ROS and mRNA expression of NLRP3. The anti-inflammatory activity of baicalin could be related to the suppression of NLRP3 inflammasome pathway under LPS stimulation.