Wear particle-mediated expressions of pro-inflammatory cytokines, NF-κB and RANK were impacted by lanthanum chloride in RAW264.7 cells
来源期刊：JOURNAL OF RARE EARTHS2013年第5期
论文作者：戴闽 江川 刘翔 李哲 程细高 邹飏 聂涛
文章页码：531 - 540
摘 要：To explore the impact of different concentrations of lanthanum chloride （LaCl3） on critical components of wear particle-mediated signaling pathways in inflammation and osteoclastogenesis, RAW264.7 cells were naturally divided into eight groups and analyzed by CCK-8 assay, flow cytometry, ELISA, RT-PCR and western blot after treatments. The results showed that three concentrations of LaCl3 had no influence on viability of RAW264.7 cells and down-regulated receptor activator of nuclear factor κB （RANK） instead of macrophage colony-stimulating factor receptor （M-CSFR）. Additionally, 2.5 and 10 μmol/L LaCl3 could signifi- cantly inhibit gene and protein levels of pro-inflammatory cytokines （tumor necrosis factor-α and interleukin-1β, i.e., TNF-α and IL-1β） and NF-κB/p65, but 100 μmol/L LaCl3 did not exert an obvious inflammation-inhibiting effect, and even induced inflammation. In conclusion, these findings demonstrated that LaCl3 was able to suppress wear particle-induced inflammation and activation of NF-κB in a certain range of concentrations in vitro and mainly decrease the expression of RANK, but not M-CSFR, all of which were generally recognized to play a pivotal role in osteoclastogenesis.
戴闽1，江川1，刘翔1，李哲1，程细高2，邹飏1，聂涛1
1. Department of Orthopaedics,The First Affiliated Hospital,Nanchang University2. Department of Orthopaedics,The Second Affiliated Hospital,Nanchang University
摘 要：To explore the impact of different concentrations of lanthanum chloride （LaCl3） on critical components of wear particle-mediated signaling pathways in inflammation and osteoclastogenesis, RAW264.7 cells were naturally divided into eight groups and analyzed by CCK-8 assay, flow cytometry, ELISA, RT-PCR and western blot after treatments. The results showed that three concentrations of LaCl3 had no influence on viability of RAW264.7 cells and down-regulated receptor activator of nuclear factor κB （RANK） instead of macrophage colony-stimulating factor receptor （M-CSFR）. Additionally, 2.5 and 10 μmol/L LaCl3 could signifi- cantly inhibit gene and protein levels of pro-inflammatory cytokines （tumor necrosis factor-α and interleukin-1β, i.e., TNF-α and IL-1β） and NF-κB/p65, but 100 μmol/L LaCl3 did not exert an obvious inflammation-inhibiting effect, and even induced inflammation. In conclusion, these findings demonstrated that LaCl3 was able to suppress wear particle-induced inflammation and activation of NF-κB in a certain range of concentrations in vitro and mainly decrease the expression of RANK, but not M-CSFR, all of which were generally recognized to play a pivotal role in osteoclastogenesis.
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