CAJ | 학술논문

目的:探讨血凝素样氧化型低密度脂蛋白受体-1(LOX-1)/核因子(NF)-κB信号途径对氧化低密度脂蛋白(ox-LDL)刺激的人脐静脉内皮细胞(HUVECs)炎症因子表达的影响及氟伐他汀的干预作用.方法:设立不同浓度的ox-LDL刺激组,LOX-1中和抗体干预组,NF-κB抑制剂吡咯烷二硫代氢基甲酸盐(PDTC)干预组,氟伐他汀干预组及空白对照组;检测细胞上清液中肿瘤坏死因子(TNF)-α,白细胞介素(IL)-6的浓度.结果:25mg/L、50mg/L、100mg/L浓度的ox-LDL刺激组24h后上清液TNF-α浓度分别为:(32.34±2.46)pg/ml、(96.43±8.36)pg/ml、(62.79±4.64) pg/ml,IL-6浓度分别为:(264.71±15.06)pg/ml、(630.70±17.77)pg/ml、(378.62±16.33)pg/ml,均较空白对照组TNF-а(22.99±3.55)pg/ml、IL-6(80.37±8.29)pg/ml水平显著升高(P<0.05～0.01);NF-кB抑制剂PDTC和LOX-1中和抗体干预后上清液TNF-α浓度较50mg/L ox-LDL刺激组显著下降(P<0.01).不同浓度氟伐他汀(0.01μmol/L、0.1μmol/L、1μmol/L)干预HUVECs 24h后上清液TNF-α浓度分别为(73.84±6.50)pg/ml、(42.59±6.45)pg/ml、(23.55±4.27)pg/ml;IL-6浓度分别为(549.0±20.23)pg/ml、(434.56±22.4)pg/ml、(302.42±21.30)pg/ml,较50mg/L ox-LDL刺激组显著下降(P<0.05～0.01).结论:氧化低密度脂蛋白可刺激人脐静脉内皮细胞上清液中炎症因子TNF-α和IL-6的表达,在25～50mg/L剂量范围内呈显著的剂量-效应关系.氟伐他汀可浓度依赖性抑制人脐静脉内皮细胞上清液中炎症因子TNF-α和IL-6的表达.
목적:탐토혈응소양양화형저밀도지단백수체-1(LOX-1)/핵인자(NF)-κB신호도경대양화저밀도지단백(ox-LDL)자격적인제정맥내피세포(HUVECs)염증인자표체적영향급불벌타정적간예작용.방법:설립불동농도적ox-LDL자격조,LOX-1중화항체간예조,NF-κB억제제필각완이류대경기갑산염(PDTC)간예조,불벌타정간예조급공백대조조;검측세포상청액중종류배사인자(TNF)-α,백세포개소(IL)-6적농도.결과:25mg/L、50mg/L、100mg/L농도적ox-LDL자격조24h후상청액TNF-α농도분별위:(32.34±2.46)pg/ml、(96.43±8.36)pg/ml、(62.79±4.64) pg/ml,IL-6농도분별위:(264.71±15.06)pg/ml、(630.70±17.77)pg/ml、(378.62±16.33)pg/ml,균교공백대조조TNF-а(22.99±3.55)pg/ml、IL-6(80.37±8.29)pg/ml수평현저승고(P<0.05～0.01);NF-кB억제제PDTC화LOX-1중화항체간예후상청액TNF-α농도교50mg/L ox-LDL자격조현저하강(P<0.01).불동농도불벌타정(0.01μmol/L、0.1μmol/L、1μmol/L)간예HUVECs 24h후상청액TNF-α농도분별위(73.84±6.50)pg/ml、(42.59±6.45)pg/ml、(23.55±4.27)pg/ml;IL-6농도분별위(549.0±20.23)pg/ml、(434.56±22.4)pg/ml、(302.42±21.30)pg/ml,교50mg/L ox-LDL자격조현저하강(P<0.05～0.01).결론:양화저밀도지단백가자격인제정맥내피세포상청액중염증인자TNF-α화IL-6적표체,재25～50mg/L제량범위내정현저적제량-효응관계.불벌타정가농도의뢰성억제인제정맥내피세포상청액중염증인자TNF-α화IL-6적표체.