目的 初步探讨系统性红斑狼疮(systemic lupus erythematosus,SLE)早发动脉粥样硬化小鼠模型的建立及评估。方法 采用载脂蛋白(apolipoprotein E,ApoE^-/-)自发性动脉粥样硬化小鼠作为研究对象,一次性腹腔注射降植烷,高脂喂养8周建立SLE早发动脉粥样硬化模型,C57BL/6小鼠注射等量生理盐水并正常喂养作为对照,检测小鼠尿素氮(blood urea nitrogen,BUN)、肌酐(creatinine, CRE)等肾功能指标及三酰甘油(triglyceride, TG)、总胆固醇(total cholesterol, TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)等血脂含量,HE染色观察小鼠肾脏组织形态改变。结果 模型鼠肌酐、尿素氮明显升高(P＜0.01),血脂指标TC由(6.52±3.40)mmol/L升高至(17.53±2.32)mmol/L,TG由(0.49±0.14)mmol/L升高至(1.03±0.21)mmol/L,LDL-C由(0.30±0.30)mmol/L升高至(1.25±0.3)mmol/L升高,差异均有统计学意义(P＜0.01),而HDL-C由(1.66±0.17)mmol/L下降至(0.79±0.17)mmol/L,差异有统计学意义(P＜0.01),同时肾脏组织炎性反应细胞浸润明显,肾小球细胞增多、肿大,显示肾脏组织病变损伤。结论 腹腔注射降植烷结合高脂喂养能成功诱导ApoE^-/-小鼠发生SLE早发动脉粥样硬化。

Objective To explore a mouse model of premature atherosclerosis in systemic lupus erythematosus (SLE). Methods Twelve-week-old ApoE^-/- mice were randomly divided into the model group and control group.The mouse model was injected with pristane intraperitoneally while the control group was injected with normal saline. After 8 weeks of high fat diet (HFD), all the animals were sacrificed, and the levels of creatinine, urea nitrogen, total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-C), and high density lipoprotein-cholesterol (HDL-C) were detected using some commercial kits. Hematoxylin (HE) staining was used to observe the morphological changes of kidney tissue. Results Compared with the control group, TC, TG, and LDL-C were increased from (6.52±3.40)mmol/L, (0.49±0.14)mmol/L and(0.30±0.30)mmol/L to (17.53±2.32) mmol/L,(1.03±0.21) mmol/L and (1.25±0.30) mmol/L respectively (P＜0.01), while the level of HDL-C was down from (1.66±0.17)mmol/L to (0.79±0.17)mmol/L (P＜0.01).The levels of creatinine and urea nitrogen were increased significantly. Meanwhile, the renal pathological damage was very severe in the model group. Conclusions A mouse model of premature atherosclerosis in SLE can be established through the intraperitoneal injection with pristane in ApoE^-/- mice, which will contribute to the treatment and prevention of premature atherosclerosis in SLE.