硫氢化钠抑制人巨噬细胞炎性因子的分泌

目的 探讨硫化氢(H2S)在人巨噬细胞炎性因子分泌中的调节作用,以深入了解H2S拮抗动脉粥样硬化的分子机制.方法 体外培养人单核细胞系THP-1细胞,经100 nmol/L佛波酯(PMA)作用24 h后使其分化为人巨噬细胞.而后将人巨噬细胞随机分为4组:对照组、氧化性低密度脂蛋白(ox-LDL) 50 mg/L组、ox-LDL+硫氢化钠(NaHS) 100及500 μmol/L干预组.对照组细胞未经ox-LDL及NaHS诱导；ox-LDL组细胞经终浓度为50 mg/Lox-LDL诱导；ox-LDL+ NaHS 100μmol/L干预组细胞经终浓度为50 mg/L ox-LDL及100μmol/L NaHS共同诱导；ox-LDL+ NaHS 500 μmol/L干预组细胞经终浓度为50 mg/L ox-LDL及500μmoL/L NaHS共同诱导.各组细胞均培养48 h后收集上清,ELISA法检测细胞上清液中肿瘤坏死因子-α(TNF-α),巨噬细胞迁移抑制因子(MIF)及白细胞介素-10(IL-10)水平.结果 与对照组相比,促炎因子TNF-α、MIF水平在ox-LDL组显著升高(P＜0.05),而抗炎因子IL-10水平显著降低(P＜0.05)；与ox-LDL组相比,TNF-α、MIF水平在ox-LDL+ NaHS 100及500μmol/L干预组明显下降(P＜0.05),而IL-10水平明显升高(P＜0.05).结论 NaHS显著抑制ox-LDL刺激的促炎因子MIF、TNF-α的分泌,而促进抗炎因子IL-10的分泌.

Sodium hydrosulfide inhibits inflammatory factor secretion in macrophages

Objective: To find out the possible effect of hydrogen sulfide (H2S) on inflammatory factor secretion in macrophage, which might help us to understand the mechanism by which H2S suppresses atherosclerosis. Methods: THP-1 monocytes were induced to differentiate into macrophages by incubation with PMA for 24 h. Then the macrophages were divided into four groups randomly: control group, oxidized low density lipoprotein (ox-LDL）50 mg/L group, ox-LDL+ sodium hydrosulfide（NaHS) 100 or 500μmol/L group. Cells in the control group were treated with neither ox-LDL nor NaHS; cells in the ox-LDL group were treated with 50 mg/L ox-LDL; cells in the ox-LDL+ NaHS 100 μmol/L group were treated with both 50 mg/L ox-LDL and 100 μmol/L NaHS; and cells in the ox-LDL+ NaHS 500 μmol/L group were treated with both 50 mg/L ox-LDL and 500 μmol/L NaHS. Cell supernatants in all the above groups were collected after induction for 48 h. ELISA was used to examine the content of tumor necrosis factor-ɑ (TNF-ɑ), interleukin-10 (IL-10) and macrophage migration inhibitory factor (MIF) in cell supernatant. Results: Compared to the control group, the content of pro-inflammatory factors-TNF-α and MIF rose significantly （P<0.05）while the content of anti-inflammatory factor IL-10 decreased significantly in the ox-LDL group（P<0.05）; compared to the ox-LDL group, the content of TNF-α and MIF decreased greatly（P<0.05） while the content of IL-10 increased significantly in the ox-LDL+ NaHS 100 or 500μmol/L group （P<0.05）. Conclusion: NaHS inhibits the secretion of pro-inflammatory factors-TNF-αand MIF but promotes the secretion of anti-inflammatory factor- IL-10 with the stimulation of ox-LDL.