Flavonoids Isolated from Flowers of Lonicera japonica Thunb. Inhibit Inflammatory Responses in BV2 Microglial Cells by Suppressing TNF‐α and IL‐β Through PI3K/Akt/NF‐kb Signaling Pathways. (18th August 2016)

• Record Type: Journal Article
• Authors: Han, Min Ho; Lee, Won Sup; Nagappan, Arulkumar; Hong, Su Hyun; Jung, Ji Hyun; Park, Cheol; Kim, Hye Jung; Kim, Gi‐Young; Kim, GonSup; Jung, Jin‐Myung; Ryu, Chung Ho; Shin, Sung Chul; Hong, Soon Chan; Choi, Yung Hyun
• Is Part Of: Phytotherapy research. Volume 30:Number 11(2016)
• Page Start: 1824
• Page End: 1832
• Publication Date: 2016-08-18
• Subjects: Lonicera japonica Thunb -- BV2 -- antiinflammatory activity -- NF‐kB -- Akt; Materia medica, Vegetable -- Periodicals; Botany, Medical -- Periodicals; Medicinal plants -- Periodicals; Plant Extracts -- therapeutic use -- Periodicals; Plants, Medicinal -- Periodicals; 581.634
• DOI: 10.1002/ptr.5688
• Languages: English
• ISSNs: 0951-418X

Abstract

Abstract : Decoctions of the dried flowers of Lonicera japonica Thunb. (Indongcho) have been utilized in folk remedies against various inflammatory diseases, and it is reported neuroprotective effects. The cytokines release from microglia is closely linked to various chronic neurodegenerative diseases like Alzheimer's disease and Parkinson's disease. It is still unknown whether the neuroprotective effects are associated with the antiinflammatory effects. Here, we determined whether polyphenols extracted from lyophilized Lonicera japonica Thunb. (PELJ) would inhibit inflammatory cytokines and mediators. We stimulated microglia with lipopolysaccharide (LPS) to produce inflammatory cytokines, and then assessed the effects of PELJ on these cytokines. PELJ significantly inhibited LPS‐induced interleukin‐1β and tumor necrosis factor‐α expressions and LPS‐induced nitric oxide (NO) and prostaglandin E2 expressions by down‐regulating inducible enzyme NO synthase and cyclooxygenase‐2 at the protein and mRNA levels. All the suppression of these mediators did not cause any significant cytotoxicity. PELJ also inhibited the nuclear translocation of nuclear factor‐kappa B and phosphorylated Akt. These findings suggest that PELJ may offer substantial therapeutic potential for treating inflammatory and neurodegenerative diseases by inhibiting pro‐inflammatory cytokines through inhibiting phosphoinositol 3‐kinase /Akt/nuclear factor‐kappa B signaling pathway. Copyright © 2016 John Wiley & Sons, Ltd.