摘要
为探讨糖基化终产物对人血管内皮细胞表达过氧化体增殖物激活型受体γ基因的影响 ,体外培养人血管内皮细胞株 (ECV30 4 ) ,分别用不同浓度葡萄糖 (0、2 0、5 0和 80mmol L)孵育的糖基化终产物修饰牛血清白蛋白(2 0 0mg L)、不同浓度的糖基化终产物修饰牛血清白蛋白 (5 0、10 0、2 0 0和 4 0 0mg L)干预 2 4h和葡萄糖浓度为 5 0mmol L孵育的糖基化终产物修饰牛血清白蛋白干预细胞 0、12、2 4、36、4 8和 72h ,逆转录聚合酶链反应检测细胞中过氧化体增殖物激活型受体γmRNA的表达水平。结果发现 ,葡萄糖浓度为 2 0、5 0和 80mmol L孵育的糖基化终产物修饰牛血清白蛋白及浓度为 5 0、10 0、2 0 0和 4 0 0mg L的糖基化终产物修饰牛血清白蛋白都减少过氧化体增殖物激活型受体γmRNA的表达 (P <0 .0 0 1) ,干预 12、2 4、36、4 8和 72h后过氧化体增殖物激活型受体γmRNA表达均较未干预组明显减少 (P <0 .0 0 1)。此结果提示 ,糖基化终产物可抑制人血管内皮细胞过氧化体增殖物激活型受体γ基因的表达。
Aim To investigate mechanism for accelerated atherosclerosis in diabetic patients, effect of advanced glycosylation end-product (AGE) on the expression of peroxisome proliferator-activated receptor-γ (PPAR γ) mRNA was observed in cultured human vascular endothelial cells (ECV304). Methods The ECV304 cells were exposed to AGE-modified bovine serum albumin (AGE-BSA) of 200 mg/L (glycated with glucose of 0, 20, 50, 80 mmol/L) for 24 h, or incubated with AGE-BSA (50 mmol/L, 200 mg/L) for 0, 12, 24, 36, 48, 72 h, and were treated by AGE-BSA (50, 100, 200, 400 mg/L) for 24 h. Expression of PPARγ mRNA in ECV304 cells was measured by RT-PCR with β-actin as internal standard. Results The expressions of PPARγ mRNA were decreased by AGE-BSA incubated with glucose concentration of 20, 50, 80 mmol/L (P<0.001) and depressed by AGE-BSA (50, 100, 200, 400 mg/L), respectively. After intervention of AGE-BSA for periods of 12, 24, 36, 48, 72 h, PPARγ mRNA expression was decreased markedly (P<0.001). Conclusion AGE-BSA could decrease the expression of PPARγ mRNA in cultured human vascular endothelial cells, which might be partly involved in atherogenesis in diabetic patients.
出处
《中国动脉硬化杂志》
CAS
CSCD
2004年第2期135-138,共4页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金 ( 3 0 0 70 3 0 0 )资助
关键词
细胞生物学
糖尿病
糖基化终产物
人血管肉皮细胞
过氧化体增殖物激活型受体Γ
基因表达
Cellular Biology
Diabetes
Glycation End Products,Advanced
Human Vascular Endothelial Cells
Peroxisome Proliferator Activated Receptor-γ
Gene Expression
