中国药物与临床
中國藥物與臨床
중국약물여림상
CHINESE REMEDIES & CLINICS
2014年
6期
721-723
,共3页
柳丽娜%贺彬%武永新%梁爽%申晓
柳麗娜%賀彬%武永新%樑爽%申曉
류려나%하빈%무영신%량상%신효
瑞舒伐他汀%氯沙坦%脂蛋白类,LDL%肝X受体
瑞舒伐他汀%氯沙坦%脂蛋白類,LDL%肝X受體
서서벌타정%록사탄%지단백류,LDL%간X수체
Rosuvastatin%Losartan%Lipoproteins,LDL%Liver X receptor
目的:探讨瑞舒伐他汀、氯沙坦联合对氧化低密度脂蛋白(ox-LDL)诱导的人单核-巨噬细胞肝X受体(LXR)表达的影响及可能的机制。方法分离并培养人单核细胞,转化为巨噬细胞。据实验要求设置空白对照组、ox-LDL模型对照组、氯沙坦组、瑞舒伐他汀组、瑞舒伐他汀联合氯沙坦组,反转录聚合酶链反应(RT-PCR)法测定各组LXR的mRNA的表达。结果与空白对照组比较,ox-LDL模型对照组LXRmRNA表达明显降低(P<0.05);氯沙坦组与ox-LDL模型对照组比较,LXRmRNA表达显著增加(P<0.05);瑞舒伐他汀组与OX-LDL模型对照组比较,LXR mRNA表达显著增加(P<0.05);瑞舒伐他汀联合氯沙坦组与ox-LDL模型对照组比较, LXR mRNA表达显著增加(P<0.05),且高于单药组(P<0.05)。结论瑞舒伐他汀、氯沙坦均可上调LXR的表达,而瑞舒伐他汀与氯沙坦以适宜剂量联合后,LXR的表达增高比单独用药更为显著。
目的:探討瑞舒伐他汀、氯沙坦聯閤對氧化低密度脂蛋白(ox-LDL)誘導的人單覈-巨噬細胞肝X受體(LXR)錶達的影響及可能的機製。方法分離併培養人單覈細胞,轉化為巨噬細胞。據實驗要求設置空白對照組、ox-LDL模型對照組、氯沙坦組、瑞舒伐他汀組、瑞舒伐他汀聯閤氯沙坦組,反轉錄聚閤酶鏈反應(RT-PCR)法測定各組LXR的mRNA的錶達。結果與空白對照組比較,ox-LDL模型對照組LXRmRNA錶達明顯降低(P<0.05);氯沙坦組與ox-LDL模型對照組比較,LXRmRNA錶達顯著增加(P<0.05);瑞舒伐他汀組與OX-LDL模型對照組比較,LXR mRNA錶達顯著增加(P<0.05);瑞舒伐他汀聯閤氯沙坦組與ox-LDL模型對照組比較, LXR mRNA錶達顯著增加(P<0.05),且高于單藥組(P<0.05)。結論瑞舒伐他汀、氯沙坦均可上調LXR的錶達,而瑞舒伐他汀與氯沙坦以適宜劑量聯閤後,LXR的錶達增高比單獨用藥更為顯著。
목적:탐토서서벌타정、록사탄연합대양화저밀도지단백(ox-LDL)유도적인단핵-거서세포간X수체(LXR)표체적영향급가능적궤제。방법분리병배양인단핵세포,전화위거서세포。거실험요구설치공백대조조、ox-LDL모형대조조、록사탄조、서서벌타정조、서서벌타정연합록사탄조,반전록취합매련반응(RT-PCR)법측정각조LXR적mRNA적표체。결과여공백대조조비교,ox-LDL모형대조조LXRmRNA표체명현강저(P<0.05);록사탄조여ox-LDL모형대조조비교,LXRmRNA표체현저증가(P<0.05);서서벌타정조여OX-LDL모형대조조비교,LXR mRNA표체현저증가(P<0.05);서서벌타정연합록사탄조여ox-LDL모형대조조비교, LXR mRNA표체현저증가(P<0.05),차고우단약조(P<0.05)。결론서서벌타정、록사탄균가상조LXR적표체,이서서벌타정여록사탄이괄의제량연합후,LXR적표체증고비단독용약경위현저。
Objective To determine the effects and putative mechanisms of rosuvastatin plus losartan on liver X receptor (LXR) expression in cultured human monocyte-macrophages induced by oxidized low-density lipoprotein (ox-LDL). Methods Human monocytes were isolated and transformed to macrophages, which were assigned to control group, ox-LDL group, losartan group, rosuvastatin group and losartan plus rosuvastatin group. The expression of LXR mRNA was assayed by using reverse transcriptase polymerase chain reaction. Results Compared with control group, the expression of LXR was atenuated in the ox-LDL group (P<0.05). Losartan group yielded higher levels of LXR ex-pression compared with ox-LDL group (P<0.05). Treatment with rosuvastatin resulted in a marked increase in LXR ex-pression (P<0.05) compared with ox-LDL group. The losartan plus rosuvastatin group was associated with markedly higher levels of LXR expression compared with the remaining groups (all P<0.05). Conclusion Losartan and rosu-vastatin, when administered alone or in combination (esp. the latter), could up-regulate the LXR expression.