title: Chondroitin sulfate extracted from the Styela clava tunic suppresses TNF-alpha-induced expression of inflammatory factors, VCAM-1 and iNOS by blocking Akt/NF-kappaB signal in JB6 cells.
abstract: Inflammatory mediators are known to play a key role in tumorigenesis, therefore, it is a promising strategy to inhibit the inflammation for cancer prevention and/or treatment. Current study was performed to investigate the effects of chondroitin sulfate (CS) extracted from Styela clava tunic on TNF-alpha-induced inflammation and to elucidate the mechanism of CS on the regulation of inflammatory factors in JB6 cells. Our results showed that CS inhibited TNF-alpha-induced NF-kappaB activation and subsequent vascular cell adhesion molecule 1 and inducible nitric oxide synthase expressions by blocking Akt signals in JB6 cells. Our results suggest that CS may be developed as an effective anti-inflammatory agent in the future.
authors.affiliation: Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
authors.forename: Cheng-Xiong
authors.initials: CX
authors.lastname: Xu
authors.forename: Hua
authors.initials: H
authors.lastname: Jin
authors.forename: Youn-Sun
authors.initials: YS
authors.lastname: Chung
authors.forename: Ji-Young
authors.initials: JY
authors.lastname: Shin
authors.forename: Min-Ah
authors.initials: MA
authors.lastname: Woo
authors.forename: Kee-Ho
authors.initials: KH
authors.lastname: Lee
authors.forename: Grace N
authors.initials: GN
authors.lastname: Palmos
authors.forename: Byeong-Dae
authors.initials: BD
authors.lastname: Choi
authors.forename: Myung-Haing
authors.initials: MH
authors.lastname: Cho
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology; D015153:Blotting, Western; D002460:Cell Line; D002470:Cell Survival; D002809:Chondroitin Sulfates / Q000302:isolation & purification / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects; D004817:Epidermis / Q000737:chemistry; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D014561:Urochordata / Q000737:chemistry*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D002809:Chondroitin Sulfates; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D051057:Proto-Oncogene Proteins c-akt