CAJ | 학술논문

目的：探讨高迁移率族蛋白1(high mobility group protein,HMGB-1)、Toll 样受体4(Toll-like receptor 4,TLR4)和血管细胞黏附因子1(vascular cell adhesion molecule-1,VCAM-1)与狼疮性肾炎(LN)血脂异常和动脉粥样硬化(atheroscleros,AS)的关系。方法收集20例正常健康人、30例系统性红斑狼疮(SLE)无肾脏损害和35例LN 患者外周静脉血,检测血脂水平、HMGB1 mRNA、TLR-4 mRNA、血清 HMGB1蛋白水平、外周血单核细胞CD14+/VCAM-1表达。结果 LN 组患者血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)明显高于 SLE 组和正常对照组(P <0.01)；LN 组患者血清中 HMGB1表达量(9.86±1.54)g/L 高于正常对照组(7.85±0.75)g/L 和 SLE 组(7.46±1.53)g/L；HMGB1 mRNA 和 TLR4 mRNA 表达亦升高(P <0.01),SLE 组和正常对照组差异无统计学意义；与 SLE 组和正常对照组比较,LN 组单核细胞中 CD14+/VCAM-1表达明显增强；在 LN 组患者外周血中 HMGB1表达与 TLR4、血脂(TG、LDL-C)呈正相关(r =0.915、0.536、0.448,P <0.05或<0.01)。结论在 LN 发病过程中晚期炎症介质 HMGB1可能通过与 TLR4结合,促进单核细胞表面 VCAM-1表达,从而引起血脂异常,参与 AS 的形成。
목적：탐토고천이솔족단백1(high mobility group protein,HMGB-1)、Toll 양수체4(Toll-like receptor 4,TLR4)화혈관세포점부인자1(vascular cell adhesion molecule-1,VCAM-1)여랑창성신염(LN)혈지이상화동맥죽양경화(atheroscleros,AS)적관계。방법수집20례정상건강인、30례계통성홍반랑창(SLE)무신장손해화35례LN 환자외주정맥혈,검측혈지수평、HMGB1 mRNA、TLR-4 mRNA、혈청 HMGB1단백수평、외주혈단핵세포CD14+/VCAM-1표체。결과 LN 조환자혈청중감유삼지(TG)、총담고순(TC)、저밀도지단백담고순(LDL-C)명현고우 SLE 조화정상대조조(P <0.01)；LN 조환자혈청중 HMGB1표체량(9.86±1.54)g/L 고우정상대조조(7.85±0.75)g/L 화 SLE 조(7.46±1.53)g/L；HMGB1 mRNA 화 TLR4 mRNA 표체역승고(P <0.01),SLE 조화정상대조조차이무통계학의의；여 SLE 조화정상대조조비교,LN 조단핵세포중 CD14+/VCAM-1표체명현증강；재 LN 조환자외주혈중 HMGB1표체여 TLR4、혈지(TG、LDL-C)정정상관(r =0.915、0.536、0.448,P <0.05혹<0.01)。결론재 LN 발병과정중만기염증개질 HMGB1가능통과여 TLR4결합,촉진단핵세포표면 VCAM-1표체,종이인기혈지이상,삼여 AS 적형성。
Objective To investigate the relationship of high mobility group protein 1 (HMGB1 ),Toll-like receptors 4(TLR-4),vascular endothelial cell adhesion molecule-1(VCAM-1)with atheroscleros(AS)and abnormality of blood lipids in lupus nephritis(LN)patients.Methods Serum samples from 65 patients including 30 patients with systemic lupus erythematosus(SLE),35 patients with LN,and 20 healthy volunteers as controls were measured in lipid profiles;HMGB1,TLR-4 mRNA expression and CD14 +/VCAM-1 in peripheral blood monocytes were detected.Results Serum triglycerides(TG),total cholesterol(TC)and low-density lipoprotein cholesterol(LDL-C)were significantly higher than those in SLE and normal control group (P < 0.01 ).The HMGB1 protein (9.86 ± 1.54)g/L in blood serum of patients with LN was higher than that in SLE(7.46 ± 1.53 )g/L and control group (7.85 ± 0.75 )g/L. HMGB1 mRNA and TLR-4mRNA expression in LN group were higher than those in SLE group and the control group (P <0.01),while there was no significant difference between SLE group and control group.The expression of VCAM-1 in CD14 + monocytes of patients with LN was higher than that of patients with SLE and normal control group.In LN peripheral blood,the HMGB1 expression showed positive correlation with TLR4 and lipids (TG,LDL-C)(r =0.91 5, 0.536,0.448,P <0.05 or <0.01).Conclusion In LN pathogenesis,HMGB1,the later inflammatory mediators,may promote the expression of monocyte cell surface VCAM-1 by binding to TLR4,causing dyslipidemia,and involved in the formation of AS.