CAJ | 학술논문

目的：观察内皮祖细胞（ EPC）对脂多糖刺激大鼠中性粒细胞（ PMN）生成肿瘤坏死因子－α（ TNF－α）、白细胞介素－1β（ IL－1β）、中性粒细胞蛋白酶（ NE）及基质金属蛋白酶－9（ MMP－9）的影响。方法分别分离培养EPC 及PMN，随机分为3组（ PBS 组、LPS组和EPC组），EPC组以1×105／孔密度将EPC接种于24孔板，贴壁后再加入同等密度的PMN，用终浓度1μg／mL的脂多糖刺激活化6 h；PBS组及LPS组中仅加入同等密度的PMN，分别给予等浓度的PBS及LPS刺激6 h；分别收集培养的上清及细胞检测各组TNF－α、IL－1β、NE及MMP－9的表达。结果 LPS组中TNF－α、IL－1β、NE及MMP－9表达较PBS组显著增加，而它们在EPC组的表达较LPS组显著降低（P＜0．05）。结论 EPC能抑制PMN的分泌功能。
목적：관찰내피조세포（ EPC）대지다당자격대서중성립세포（ PMN）생성종류배사인자－α（ TNF－α）、백세포개소－1β（ IL－1β）、중성립세포단백매（ NE）급기질금속단백매－9（ MMP－9）적영향。방법분별분리배양EPC 급PMN，수궤분위3조（ PBS 조、LPS조화EPC조），EPC조이1×105／공밀도장EPC접충우24공판，첩벽후재가입동등밀도적PMN，용종농도1μg／mL적지다당자격활화6 h；PBS조급LPS조중부가입동등밀도적PMN，분별급여등농도적PBS급LPS자격6 h；분별수집배양적상청급세포검측각조TNF－α、IL－1β、NE급MMP－9적표체。결과 LPS조중TNF－α、IL－1β、NE급MMP－9표체교PBS조현저증가，이타문재EPC조적표체교LPS조현저강저（P＜0．05）。결론 EPC능억제PMN적분비공능。
Objective To explore the influence of endothelial progenitor cells ( EPC ) on polymorphonuclear cells (PMN) secretory factors stimulated by lipopolysaccharide (LPS).Methods EPC and PMN were separated and cultured respectively , and they were divided into three groups .EPC were incubated in a 24-well plate at a density of 1 ×105 per well.After adherence, PMN with the same density were added in the medium , and 1μg/mL LPS was applied to the mixture for 6 hours.There are same density PMN in PBS and LPS groups stimulated by equidensity PBS and LPS respectively . Supernatant and cells were collected for determination , and the changes of tumor necrosis factor -α(TNF-α), interleukin-1β(IL-1β), neutrophil elastase (NE) and matrix metalloproteinases -9 (MMP-9) in three groups were detected .Results TNF-α, IL-1β, NE and MMP-9 contents were remarkably increased with stimulated by LPS compared with PBS group (P<0.05).When EPC were added, all productions significantly reduced ( P <0.05 ).Conclusion EPC can inhabit the activation of PMN after stimulating with LPS .