title: Anti-inflammatory effects of farrerol on IL-1β-stimulated human osteoarthritis chondrocytes.
abstract: The present study aimed to investigate the anti-inflammatory effects and the underlying molecular mechanism of farrerol on IL-1β-stimulated human osteoarthritis chondrocytes. Chondrocytes were pretreated with farrerol 1h before IL-1β stimulation. The effects of farrerol on NO and PGE2 production were tested by Griess reagent and ELISA. The effects of farrerol on COX-2, iNOS, Akt, phosphorylated Akt, and NF-κB activation were measured by western blot analysis. The results showed that farrerol remarkably inhibited IL-1β-induced NO and PGE2 production, as well as COX-2 and iNOS expression. Farrerol also inhibited IL-1β-induced NF-κB activation. Furthermore, farrerol significantly inhibited IL-1β-induced phosphorylation of PI3K and Akt. In conclusion, these results indicated that farrerol inhibited IL-1β-induced inflammatory responses in osteoarthritis chondrocytes by blocking PI3K/Akt/NF-κB signaling pathway.
authors.affiliation: Department of Orthopedics, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, China. Electronic address: zhanghongfeigz@163.com.
authors.forename: Hongfei
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Orthopedics, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, China.
authors.forename: Jiapeng
authors.initials: J
authors.lastname: Yan
authors.affiliation: Department of Orthopedics, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, China.
authors.forename: Yuesheng
authors.initials: Y
authors.lastname: Zhuang
authors.affiliation: Department of Orthopedics, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261031, China.
authors.forename: Guiquan
authors.initials: G
authors.lastname: Han
mesh_terms: D000368:Aged; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002867:Chromones / Q000494:pharmacology*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology*; D008875:Middle Aged; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D020370:Osteoarthritis, Knee / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D002867:Chromones; C508585:IL1B protein, human; D053583:Interleukin-1beta; D016328:NF-kappa B; C015881:farrerol; D009569:Nitric Oxide; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt; D015232:Dinoprostone
keywords: Farrerol; IL-1β; NF-κB; Osteoarthritis chondrocyte; PI3K