中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2009年
8期
630-634
,共5页
钱一欣%倪兆慧%顾乐怡%戴慧莉%严玉澄%张伟明%王玲%俞赞喆%吴青伟%钱家麒
錢一訢%倪兆慧%顧樂怡%戴慧莉%嚴玉澄%張偉明%王玲%俞讚喆%吳青偉%錢傢麒
전일흔%예조혜%고악이%대혜리%엄옥징%장위명%왕령%유찬철%오청위%전가기
糖尿病%动脉硬化%肝X受体%三磷酸腺苷结合盒转运子A1
糖尿病%動脈硬化%肝X受體%三燐痠腺苷結閤盒轉運子A1
당뇨병%동맥경화%간X수체%삼린산선감결합합전운자A1
Diabetes mellitus%Arteriosclerosis%Liver X receptor%ATP-binding cassette transporter A1
目的 探讨高糖对人THP-1巨噬细胞肝X受体(LXR)和二磷酸腺苷结合盒转运子A1(ABCA1)表达的影响.方法 人THP-1单核细胞经佛波脂(PMA)诱导转化成巨噬细胞.用CD68检测巨噬细胞表面标志物表达.以不同浓度葡萄糖(5.6、11.1、22.2、33.3mmol/L)和不同时间(0、0.5、2、6、12、24、48、72 h)刺激巨噬细胞,用实时荧光定量PCR法检测其LXRα、LXRβ、ABCA1 mRNA表达;Western印迹法检测LXRα、LXβ和ABCA1蛋白的表达,并分析其相互间作用.结果 PMA诱导72 h后,TPH-1细胞CD68呈阳性表达.与正常浓度糖(5.6 mmol/L)刺激比较.高糖刺激24 h后,TPH-1巨噬细胞LXR和ABCA1 mRNA和蛋白表达均下调.高糖刺激30 min后,LXRα、LXRβ和ABCA1 mRNA和蛋白表达上调;2 h后开始下调,随着时间延长而逐渐减少.结论 高糖可能通过抑制LXR和ABCA1的表达,参与了动脉粥样硬化的发生和发展.
目的 探討高糖對人THP-1巨噬細胞肝X受體(LXR)和二燐痠腺苷結閤盒轉運子A1(ABCA1)錶達的影響.方法 人THP-1單覈細胞經彿波脂(PMA)誘導轉化成巨噬細胞.用CD68檢測巨噬細胞錶麵標誌物錶達.以不同濃度葡萄糖(5.6、11.1、22.2、33.3mmol/L)和不同時間(0、0.5、2、6、12、24、48、72 h)刺激巨噬細胞,用實時熒光定量PCR法檢測其LXRα、LXRβ、ABCA1 mRNA錶達;Western印跡法檢測LXRα、LXβ和ABCA1蛋白的錶達,併分析其相互間作用.結果 PMA誘導72 h後,TPH-1細胞CD68呈暘性錶達.與正常濃度糖(5.6 mmol/L)刺激比較.高糖刺激24 h後,TPH-1巨噬細胞LXR和ABCA1 mRNA和蛋白錶達均下調.高糖刺激30 min後,LXRα、LXRβ和ABCA1 mRNA和蛋白錶達上調;2 h後開始下調,隨著時間延長而逐漸減少.結論 高糖可能通過抑製LXR和ABCA1的錶達,參與瞭動脈粥樣硬化的髮生和髮展.
목적 탐토고당대인THP-1거서세포간X수체(LXR)화이린산선감결합합전운자A1(ABCA1)표체적영향.방법 인THP-1단핵세포경불파지(PMA)유도전화성거서세포.용CD68검측거서세포표면표지물표체.이불동농도포도당(5.6、11.1、22.2、33.3mmol/L)화불동시간(0、0.5、2、6、12、24、48、72 h)자격거서세포,용실시형광정량PCR법검측기LXRα、LXRβ、ABCA1 mRNA표체;Western인적법검측LXRα、LXβ화ABCA1단백적표체,병분석기상호간작용.결과 PMA유도72 h후,TPH-1세포CD68정양성표체.여정상농도당(5.6 mmol/L)자격비교.고당자격24 h후,TPH-1거서세포LXR화ABCA1 mRNA화단백표체균하조.고당자격30 min후,LXRα、LXRβ화ABCA1 mRNA화단백표체상조;2 h후개시하조,수착시간연장이축점감소.결론 고당가능통과억제LXR화ABCA1적표체,삼여료동맥죽양경화적발생화발전.
Objective To investigate the effect of high glucose on the expression of liver X receptors (LXRs) and ATP-binding cassette transporter A1 (ABCA1) in human macrophages (THP-1 cell line). Methods THP-1 monocytes were differentiated into macrophages by induction of phorbol 12, 13-dibutyrate (PMA). Surface markers of macrophages were identified by CD68 immunohistochemistry. The macrophages were cultured with different concentration (5.6, 11.1, 22.2 and 33.3 mmol/L) of glucose and different time (0, 0.5, 2, 6, 12, 24, 48, 72 h). Real time PCR and Western blotting methods were used to examine the mRNA and protein expression of LXRs and ABCA1. Results As compared to 5.6 mmol/L glucose, macrophage LXRβ and ABCA1 were decreased significantly at both mRNA and protein levels in dose-and time-dependent manner (P<0.05). Conclusion Hyperglycemia may play a role in the pathogenesis of arteriosclerosis through the inhibition of LXRs and ABCA1 expression in diabetic patients.
