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目的探讨低密度脂蛋白受体相关蛋白(low density lipoprotein receptor-related protein,LRP1)、清道夫受体CD36、SR-A在脂质诱导肾脏损伤中的作用。方法雄性ApoE/CD36/SR-A三敲除小鼠12只,按随机数字表法分为普通组和高脂组。检测血清淀粉样蛋白(serum amyloid A protein,SAA),IL-6、脂质水平及尿蛋白。油红“O”染色及酶法检测肾组织内脂质沉积情况。HE、过碘酸-希夫(periodic acid Schiff reaction,PAS)、马松(Masson)方法观察肾脏形态学改变,定量PCR技术,Western blot与免疫组化技术检测肾组织相关因子水平。结果高脂组脂质水平[TC(51.96±5.60)、LDL(16.79±4.80)mmol/L]显著高于普通组[TC(18.11±3.07)、LDL(3.27±1.79)mmol/L](P<0.05)。肾脏脂质的沉积明显升高,高脂组尿蛋白[(2.90±0.50)mg/ml]显著高于普通组[(1.85±0.18)mg/ml](P<0.05),肾脏病理改变显著,进一步检测发现高脂组上调了LRP1(增高2.23倍)、肾脏Ⅰ型胶原蛋白、转化生长因子(TGF-β)、纤维连接蛋白(Fibronectin)mRNA与蛋白的表达。结论 LRP1可能参与肾脏泡沫细胞的形成及肾脏的损伤,SR-A,CD36不能解释泡沫细胞形成的全部机制。
Objective To investigate the role of low density lipoprotein receptor-related protein (LRP1), scavenger receptor (CD36) and SR-A in lipid-induced renal injury. Methods Twelve male ApoE / CD36 / SR-A triple knockout mice were randomly divided into normal group and high fat group according to random number table. Serum amyloid A protein (SAA), IL-6, lipid levels and urine protein were detected. Oil red “O ” staining and enzymatic detection of lipid deposition in renal tissue. HE, periodic acid Schiff reaction (PAS) and Masson method were used to observe the morphological changes of kidney. Quantitative PCR, Western blot and immunohistochemistry were used to detect the levels of renal related factors. Results Lipid levels (TC (51.96 ± 5.60), LDL (16.79 ± 4.80) mmol / L] were significantly higher in the hyperlipidemic group than in the normal group [TC (18.11 ± 3.07) and LDL [3.27 ± 1.79 mmol / L] <0.05). (2.90 ± 0.50) mg / ml] was significantly higher than that of the common group [(1.85 ± 0.18) mg / ml] (P <0.05). The renal pathological changes were significant, Further tests showed that the expression of mRNA and protein of type Ⅰ collagen, transforming growth factor (TGF-β) and fibronectin in kidney was up-regulated in high-fat diet group. Conclusion LRP1 may be involved in the formation of renal foam cells and kidney damage. SR-A and CD36 can not explain the whole mechanism of foam cell formation.