Protein Information

ID 2450
Name interleukin 1beta
Synonyms Catabolin; IL 1; IL 1 beta; IL 1B; IL1 beta; IL1B; IL1F2; Interleukin 1…

Compound Information

ID 1402
Name methylene chloride
CAS dichloromethane

Reference

PubMed Abstract RScore(About this table)
20093788 Yoon T, Cheon MS, Lee AY, Lee do Y, Moon BC, Chun JM, Choo BK, Kim HK: Anti-inflammatory activity of methylene chloride fraction from Glehnia littoralis extract via suppression of NF-kappaB and mitogen-activated protein kinase activity. J Pharmacol Sci. 2010 Jan;112(1):46-55.
Glehnia littoralis (Umbelliferae) has been used traditionally in Korean, Japanese, and Chinese medicine for the treatment of immune-related diseases; however, its anti-inflammatory activity and underlying mechanism remain to be defined. We investigated the anti-inflammatory effect and inhibitory mechanism on inflammation by the methylene chloride fraction from Glehnia littoralis extract (MCF-GLE), which was more effective than Glehnia littoralis extract (GLE). MCF-GLE inhibited 12-O-Tetradecanoyl-phorbol-13-acetate (TPA)-induced inflammation in an inflammatory edema mouse model. Also, MCF-GLE strongly inhibited the releases of nitric oxide (NO), prostaglandin E (2) (PGE (2)), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) and significantly suppressed the mRNA and protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in lipopolysaccharide-stimulated RAW 264.7 macrophage cells in a dose-dependent manner. Furthermore, MCF-GLE suppressed NF-kappaB activation and IkappaB-alpha degradation. MCF-GLE also attenuated the activation of ERK and JNK in a dose-dependent manner. These results indicate that MCF-GLE has an inhibitory effect on the in vivo and in vitro inflammatory reaction and is a possible therapeutic agent. Our results suggest that the anti-inflammatory properties of MCF-GLE may result from the inhibition of pro-inflammatory mediators, such as NO, PGE (2), TNF-alpha, and IL-1beta via suppression of NF-kappaB- and mitogen-activated protein kinases-dependent pathways.
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