摘要
目的 探讨阿托伐他汀对脂肪细胞参与脂质代谢和分泌炎症介质的影响及其机制。方法 将新西兰兔皮下脂肪细胞分别在含阿托伐他汀 (0~ 10 μmol/L)的培养基中孵育 2 4h ,用酶联免疫吸附法 (ELISA)检测上清液中白介素 6 (IL 6 )水平 ;使用半定量逆转录聚合酶链式反应 (RT PCR)检测过氧化物酶增殖体激活受体 (PPAR)γ、清道夫受体 (CD36 )mRNA的表达。测定脂肪细胞对12 5I OxLDL的特异性摄取量 ,并观察阿托伐他汀对其干预作用。结果 正常脂肪细胞可摄取12 5I OxLDL。阿托伐他汀可剂量依赖性的降低脂肪细胞分泌IL 6 ,并增加其对12 5I OxLDL的摄取 ,同时亦可剂量依赖性增加脂肪细胞PPARγ和CD36mRNA的表达。脂肪细胞分泌IL 6与其PPARγmRNA表达呈显著负相关 (r =- 0 6 3,P =0 0 11) ,同时脂肪细胞对12 5I OxLDL的特异性摄取量与PPARγ和CD36mRNA的表达呈显著正相关 (r =0 84、0 89,P均 <0 0 1)。结论 脂肪细胞既可分泌促炎症因子又可摄取Ox LDL ,阿托伐他汀可通过影响PPARγ和CD36mRNA的表达而调节脂肪细胞分泌IL 6和摄取Ox LDL的功能。
Objective To explore the influence and possible mechanism of atorvastatin on interleukine-6 (IL-6) secretion and oxidized low-density lipoprotein (Ox-LDL) uptake in primary cultured adipocytes. Methods Subcutaneous adipose was collected from groin of healthy male rabbits under deep anesthesia for adipocytes culture. Adipocytes were incubated with atorvastatin (0 up to 10 μmol/L) for 24 hours. IL-6 production was detected by enzyme link immunosorbent assay (ELISA). The specific uptake of Ox-LDL in adipocytes was measured by gamma counter and normalized to the cell protein concentration. Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate PPARγ and CD36 mRNA expressions. Results Primary cultured adipocytes dose-dependently uptook 125I-OxLDL. Atorvastatin enhanced the specific uptake of 125I-OxLDL and inhibited the IL-6 secretions in adipocytes in dose-dependent manner. Additionally, atorvastatin intervention resulted in the upregulated PPARγ and CD36 mRNA expressions in adipocytes. The effect of atorvastatin on IL-6 secretion was negatively correlated with the upregulation of PPARγ mRNA expression (r=-0.63, P=0.011), meanwhile the specific uptake of 125I-OxLDL in atorvastatin treated adipocytes was significantly related to mRNA expressions of PPARγ and CD36 receptor (r=0.84 and 0.89 respectively,P< 0.01). Conclusion The results demonstrate that adipocytes can uptake Ox-LDL. Atorvastatin inhibits IL-6 secretion and enhances Ox-LDL uptake in adipocytes, which may ascribe to the upregulated mRNA expressions of PPARγ and CD36.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2003年第11期855-858,共4页
Chinese Journal of Cardiology
基金
国家自然科学基金资助 ( 3 9970 2 96)