CAJ | 학술논문

目的：观察薯蓣皂苷片对类风湿性关节炎细胞模型核转录因子NF-资Bp65及基质金属蛋白酶-9（MMP-9）、血管内皮生长因子（VEGF）、肿瘤坏死因子α（TNF-α）表达的影响。方法：用白介素-17（IL-17）+TNF-α共同孵育大鼠RSC-364细胞，以不同浓度薯蓣皂苷片进行干预，MTT法检测不同药物浓度对细胞存活率影响，采用Western blot检测各组NF-资Bp65及其抑制蛋白（I资B-α）的表达，酶联免疫吸附试验（ELISA）检测细胞培养液上清中VEGF、MMP-9、TNF-α蛋白水平的变化。结果：薯蓣皂苷片可促进资B抑制蛋白的表达量，降低NF-资B蛋白水平的高表达，并降低细胞分泌VEGF、MMP-9、TNF-α水平。结论：薯蓣皂苷片对RSC-364细胞核因子资B有负向调节作用，提升I资B-α的表达并能降低炎性因子和血管新生因子分泌，提示其在类风湿发病中可能起到潜在的调节作用。
목적：관찰서여조감편대류풍습성관절염세포모형핵전록인자NF-자Bp65급기질금속단백매-9（MMP-9）、혈관내피생장인자（VEGF）、종류배사인자α（TNF-α）표체적영향。방법：용백개소-17（IL-17）+TNF-α공동부육대서RSC-364세포，이불동농도서여조감편진행간예，MTT법검측불동약물농도대세포존활솔영향，채용Western blot검측각조NF-자Bp65급기억제단백（I자B-α）적표체，매련면역흡부시험（ELISA）검측세포배양액상청중VEGF、MMP-9、TNF-α단백수평적변화。결과：서여조감편가촉진자B억제단백적표체량，강저NF-자B단백수평적고표체，병강저세포분비VEGF、MMP-9、TNF-α수평。결론：서여조감편대RSC-364세포핵인자자B유부향조절작용，제승I자B-α적표체병능강저염성인자화혈관신생인자분비，제시기재류풍습발병중가능기도잠재적조절작용。
This study was aimed to observe the influence of Discornin Tablets on activation nuclear transcription factor NF-κBp65 of rheumatoid arthritis (RA) cell model as well as the expression of MMP-9, VEGF and tumor necrosis factor-α (TNF-α). Interleukin-17 (IL-17) and TNF-α were used for stimulating RSC-364 cells. Discornin Tablets at different concentrations were used for intervention. The influence of Discornin Tablets in different concentrations on cell viability was detected by MTT method. Expressions of NF-κBp65 and its inhibitory protein (IκB-α) in each group were detected by western blot method. Changes in VEGF, MMP-9 and TNF-α protein levels in cell broth supernatant were checked by ELISA. The results showed that Discornin Tablets can promote the expression of κB inhibitory pro-tein, reduce the high expression of NF-κB protein level, and inhibit the cellular secretion of VEGF, MMP-9 and TNF-α. It was concluded that Discornin Tablets had negative regulation effect on nuclear transcription factor κB of RSC-364 cells. It can increase the expression of IκB-α, as well as reduce the secretion of inflammation factors and blood vessel newborn factors. It suggested that Discornin Tablets may have the potential regulation effect on RA.