Glycyrrhizin inhibits interleukin-8 production and nuclear factor-kappaB activity in lung epithelial cells, but not through glucocorticoid receptors
This study was designed to examine the glucocorticoid-like inhibitory effect of glycyrrhizin (GL) on interleukin (IL)-8 production in A549 lung epithelial cells. GL, as well as dexamethasone (DEX) inhibited both tumor necrosis factor (TNF)-alpha- and IL-1beta-induced IL-8 production, mRNA expression...
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| Veröffentlicht in: | Journal of pharmacological sciences 2008-03, Vol.106 (3), p.460-468 |
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| container_title | Journal of pharmacological sciences |
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| creator | Takei, Hironori Baba, Yuichiro Hisatsune, Akinori Katsuki, Hiroshi Miyata, Takeshi Yokomizo, Kazumi Isohama, Yoichiro |
| description | This study was designed to examine the glucocorticoid-like inhibitory effect of glycyrrhizin (GL) on interleukin (IL)-8 production in A549 lung epithelial cells. GL, as well as dexamethasone (DEX) inhibited both tumor necrosis factor (TNF)-alpha- and IL-1beta-induced IL-8 production, mRNA expression, and promoter activity in A549 cells. Both GL and DEX inhibited transactivation of nuclear factor (NF)-kappaB, without inhibiting translocation of the NF-kappaB p65 subunit to the nucleus. However, the effect of GL was insensitive to RU486, a GR antagonist, and to GR knockdown by siRNA. Furthermore, only GL inhibited DNA binding of p65 to the IL-8 promoter region. These findings indicated that GL had a glucocorticoid-like inhibitory effect on IL-8 production via a mechanism that differs from that of glucocorticoids. |
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GL, as well as dexamethasone (DEX) inhibited both tumor necrosis factor (TNF)-alpha- and IL-1beta-induced IL-8 production, mRNA expression, and promoter activity in A549 cells. Both GL and DEX inhibited transactivation of nuclear factor (NF)-kappaB, without inhibiting translocation of the NF-kappaB p65 subunit to the nucleus. However, the effect of GL was insensitive to RU486, a GR antagonist, and to GR knockdown by siRNA. Furthermore, only GL inhibited DNA binding of p65 to the IL-8 promoter region. 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GL, as well as dexamethasone (DEX) inhibited both tumor necrosis factor (TNF)-alpha- and IL-1beta-induced IL-8 production, mRNA expression, and promoter activity in A549 cells. Both GL and DEX inhibited transactivation of nuclear factor (NF)-kappaB, without inhibiting translocation of the NF-kappaB p65 subunit to the nucleus. However, the effect of GL was insensitive to RU486, a GR antagonist, and to GR knockdown by siRNA. Furthermore, only GL inhibited DNA binding of p65 to the IL-8 promoter region. These findings indicated that GL had a glucocorticoid-like inhibitory effect on IL-8 production via a mechanism that differs from that of glucocorticoids.</abstract><cop>Japan</cop><pmid>18344608</pmid><tpages>9</tpages></addata></record> |
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| ispartof | Journal of pharmacological sciences, 2008-03, Vol.106 (3), p.460-468 |
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| language | eng |
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| source | J-STAGE Free; MEDLINE; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | Active Transport, Cell Nucleus Anti-Inflammatory Agents - pharmacology Cell Line, Tumor DNA - metabolism Epithelial Cells - drug effects Glycyrrhizic Acid - pharmacology Humans Interleukin-8 - biosynthesis Interleukin-8 - genetics Lung Promoter Regions, Genetic Receptors, Glucocorticoid - drug effects Receptors, Glucocorticoid - physiology Transcription Factor RelA - metabolism |
| title | Glycyrrhizin inhibits interleukin-8 production and nuclear factor-kappaB activity in lung epithelial cells, but not through glucocorticoid receptors |
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