Effect of CD14, Toll-like receptors, cytoskeletal inhibitors and NF-kappaB inhibitor on MMP-8 release from human neutrophils induced by E. coli lipopolysaccharides / 대한치주과학회지

OBJECTIVE: MMP-8 is a neutrophil enzyme and its level increases in some inflammatory diseases, including periodontal disease. We knew that the lipopolysaccharide of E.coli(E-LPS) induced MMP-8 release from human neutrophils. E-LPS is known to induce the production and release of inflammatory cytokines through CD14, Toll-like receptor(TLR). In the present study, we investigated whether MMP-8 release by E-LPS is induced via CD14-TLR pathway and the cellular mechanism of MMP-8 release in human neutrophils. MATERIAL AND METHODS: Human neutrophils were isolated from the peripheral blood of healthy donors and pre-incubated in medium containing antibodies against CD14, anti-TLR2 and anti-TLR4 or several inhibitors of microtubules and microfilaments and then incubated with E-LPS. The cells were treated TPCK and E-LPS simultaneously. The MMP-8amount in the culture medium was determined using ELISA. RESULTS: E-LPS increased MMP-8release from neutrophils and its induction was inhibited by anti- CD14 and anti-TLR4 but not by anti-TLR2 antibodies. The inhibitors of micro- tubule and microfilament polymerization significantly decreased E-LPS-induced MMP- 8release. TPCK inhibited E-LPS-induced MMP-8 release. CONCLUSION: These results suggest that MMP-8 release is induced by E-LPS via the CD14-TLR4 signal pathway in human neutrophils and may be depedent on microtubule and microfilament systems and NF-kappaB pathway.

Effect of NF-?B inhibitor pyrrolidine dithiocarbonate on the proliferation and apoptosis in K562 cells / 中国病理生理杂志

AIM:To investigate the effect of pyrrolidine dithiocarbamate (PDTC),a specific inhibitor of NF-?B on the proliferation and apoptosis of K562 cells and to explore the anti-tumor mechanism of PDTC.METHODS:Trans AMTM NF-?B p65 kit was used to detect the activity of p65 in K562 cells treated by PDTC. The effect of PDTC on the proliferation of K562 cells was measured by WST-1 method. DNA damage was detected by single cell gel electrophoresis (comet assay). The procaspase-3 and activated protein level of caspase-3 were detected by Western blotting.RESULTS:The activity of p65 in K562 cells was inhibited after treated by PDTC (P