Propargyl-PEG2-N-bis(PEG2) - CAS 2100306-62-3

Objective:This study was aimed to explore effect of baicalin on IKK/IKB/NF-kB signaling pathway and apoptosis-related proteins in rats with ulcerative colitis (UC). Methods:Histopathological observation and scores of colon tissue were performed in the UC rat model. IKK/IKB/NF-kB signaling pathway and apoptosis-related proteins were measured by Western blotting. Results:Baicalin significantly increased the activity of SOD, CAT and GSH-Px in colon tissue of rats with UC, but significantly decreased the content of MDA, IL-1β, MPO, PEG2 and TNF-α in colon tissue of rats with UC. In the molecular mechanism, baicalin significantly decreased the expression of cleaved-caspase3, cleaved-caspase9, Bcl-2/Bax, cyt-c, NF-kB p-65, p-IKKβ/IKKβ and p-IKBα/IKBα. Baicalin could significantly inhibit p-IKBα/IKBα content change, but had no significant effect on p-IKKβ/IKKβ.Conclusion:Baicalin may have a regulating effect on IKK/IKB/NF-kB signaling pathway and apoptosis-related proteins in UC rats.

Ethnopharmacological relevance:Pteryxin is a natural coumarin compound that is found in "Qianhu", a traditional Chinese medicine, which possesses heat-clearing and detoxifying functions according to the theory of Traditional Chinese Medicine. Despite its medicinal effects, its anti-inflammatory and mechanisms of actions have not been established.Aim of this study:This study aims to evaluate the anti-inflammatory property and reveal the possible anti-inflammatory mechanisms of pteryxin.Material and methods:LPS-induced RAW 264.7 macrophages and LPS-induced zebrafish model were used for the anti-inflammatory activity determination of pteryxin. The level of NO, PEG2, TNF-α and IL-6 were measured by ELISA. The accumulation of NO and ROS was stained and observed by a fluorescence microscopy. The nuclear translocation of NF-κB p65 and formation of NLRP3 inflammasome complex in LPS-induced RAW 264.7 macrophage cells were analyzed by immunofluorescence assay. The expression level of iNOS, IL-6, COX-2, TNF-α, p-p38, p38, ERK, JNK, p-ERK, p-JNK, IKK, IκB-α, p-IKK, p-IκB-α, p65, NLRP3, p-p65, Caspase 1 (p 20), ASC, and GAPDH were determined by Western blotting. Results:Lipopolysaccharide (LPS)-induced prostaglandin E2 (PGE2) and nitric oxide (NO) secretions were found to be downregulated by pteryxin. Moreover, pteryxin significantly suppressed inflammatory factor secretion in LPS-treated RAW 264.7 cells. Mechanistically, pteryxin significantly downregulated NF-κB/MAPK activation. Moreover, pteryxin inhibited caspase-1 and NLRP3 activation and formation of ASC specks in RAW 264.7 cells, implying that pteryxin inhibits inflammasome assembly, which is a signal for NLRP3 inflammasome activation. In conclusion, pteryxin blocks NF-κB/MAPK signaling, and suppresses the initiation and activation of NLRP3 thereby preventing inflammation.Conclusion:Pteryxin is a potential treatment option for inflammatory-related diseases.

Solute carrier (SLC) transporters meditate many essential physiological functions, including nutrient uptake, ion influx/efflux, and waste disposal. In its protective role against tumors and infections, the mammalian immune system coordinates complex signals to support the proliferation, differentiation, and effector function of individual cell subsets. Recent research in this area has yielded surprising findings on the roles of solute carrier transporters, which were discovered to regulate lymphocyte signaling and control their differentiation, function, and fate by modulating diverse metabolic pathways and balanced levels of different metabolites. In this review, we present current information mainly on glucose transporters, amino-acid transporters, and metal ion transporters, which are critically important for mediating immune cell homeostasis in many different pathological conditions.