Purpose: To investigate the mechanism by which pinitol inhibits tumor necrosis factor-α (TNF-α)-induced expression of matrix

Purpose: This study is aimed at identifying the anti-inflammatory mechanisms of a methanol extract of Polyopes lancifolius (MEPL) in lipopolysaccharide (LPS)-stimulated BV2 microglia cells. Methods: The expression of mRNA and protein were investigated RT-PCR and western blot analyses in LPS-stimulated BV2 microglial cells. The level of nitric oxide (NO) production was analyzed using Griess reaction. The release of prostaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) were determined using sandwich ELISA. NF-κB activation was detected using EMSA methods. Results: MEPL significantly suppressed NO production in LPS-stimulated BV2 cells without any cytotoxicity. The results also indicate that MEPL decreased the production of PGE2 and TNF-α in LPSstimulated BV2 cells. Furthermore, pretreatment with MEPL resulted in a downregulation of LPSinduced mRNA and protein expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) and TNF-α. Investigation of the effect of MEPL on nuclear factor-κB (NF-κB) activity, which is a potential transcriptional factor for regulating inflammatory genes such as iNOS, COX-2 and TNF-α, showed that MEPL substantially inhibited the LPS-induced DNA-binding activity of NF-κB. MEPL also suppressed the LPS-induced degradation and phosphorylation of IκBα, and it consequently blocked p65 translocation from the cytosol to the nucleus. Conclusion:These data show that MEPL may regulate LPS-induced NO, PGE2, and TNF-α production by suppressing NF-κB activity.

Purpose: Hydroclathrus clathratus is a brown marine seaweed known to possess anti-cancer, anti-herpetic, and anti-coagulant activities. The present study is aimed at investigating some anti-inflammatory effects of H. clathratus. Methods: We investigated the anti-inflammatory effects of the methanol extract of H. clathratus (MEHC) by expression of mRNA and protein using RT-PCR and Western blot analysis in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. The level of nitric oxide (NO) production was analyzed using Griess reaction.The release of prostaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) were determined using sandwich ELISA. NF-κB activation was detected using EMSA methods. Results: The results obtained indicate that the extract (MEHC) inhibited LPS-induced NO, PGE2, and TNF-α production without any significant cytotoxicity (p < 0.05). MEHC also inhibited production of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) and TNF-α mRNA in LPS-stimulated BV2 microglial cells. In addition, MEHC significantly reduced (p < 0.05) nuclear translocation of the nuclear factor-κB (NF-κB) subunits, p50 and p65, and its DNA-binding activity in LPS-stimulated BV2 microglial cells. Conclusion: These results suggest that MEHC suppresses the induction of TNF-α, as well as iNOS and COX-2 expression, by blocking LPS-induced NF-κB activation.

Purpose: To elucidate the anti-inflammatory mechanisms of aqueous extract of Oldenlandia diffusa (AEOD) in cells. LPS-induced mRNA and protein expression of iNOS, COX-2 and TNF-α were attenuated by treatment with AEOD. These data imply that AEOD tightly regulates the expression of these inflammatory mediators at the transcriptional level. Therefore, we determined the effects of AEOD on nuclear factor-κB (NF-κB) activity, which has been considered to be a potential transcriptional factor for regulating the expression of iNOS, COX-2 and TNF-α. As expected, AEOD suppressed the LPS-induced degradation and phosphorylation of

Purpose: To investigate the effects of the methanol extract of Polyopes lancifolius (MEPL) on the expression of matrix metalloproteinase-9 (MMP-9) and invasion in T24 human bladder carcinoma cells. Methods: Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analyses were performed to assess the expression of MMP-9 and its regulatory proteins. MMP-9 activity was evaluated using zymography while matrigel infiltration was performed to assess T24 bladder carcinoma invasion. Electrophoretic mobility assay was used to investigate the nuclear factor-κB (NF-κB) activity. Results: The expression and activity of MMP-9 were significantly increased in response to TNF-α, but MEPL suppressed TNF-α-induced MMP-9 expression and activity. MEPL also inhibited TNF-α-induced MMP-9 expression at the transcriptional level by blocking the activation of the NF-κB signaling pathway. Furthermore, the extract suppressed TNF-α-induced phosphorylation of IκBα and consequently sustained cytosolic p65 and p50 expression. Matrigel invasion assay showed that MEPL significantly reduced TNF-α-induced invasion of T24 bladder carcinoma cells. Conclusion: Collectively, these data indicate that MEPL regulates TNF-α-induced MMP-9 expression by suppressing NF-κB activity.