大鼠动脉钙化诱导过程中炎症小体复合物分子的变化  

Involvement of Inflammasome Complex During Rat Arterial Calcification in vivo

作　　者：彭利静[1] 李慧[1] 李超民[1] 

机构地区：[1]解放军第451医院心血管内科,陕西西安710054

出　　处：《生物技术通讯》2014年第3期388-390,共3页Letters in Biotechnology

摘　　要：目的:以SD大鼠动脉钙化为模型,研究钙化发生过程中炎症小体复合物分子的变化。方法:大鼠皮下注射维生素D3诱导动脉钙化,并用HE染色检测动脉钙化的发生,用半定量PCR测定钙化发展过程中细胞内NALP3炎症小体复合物核心蛋白NALP3、ASC和Caspase-1的mRNA水平变化。结果:随着动脉钙化的发展,细胞内NALP3、ASC和Caspase-1的mRNA表达水平逐步增加。结论:构建了大鼠动脉钙化模型,并且发现NALP3炎症小体复合物在动物钙化诱导过程中表达增加,为进一步研究动脉钙化的机制及筛选抗动脉硬化药物打下基础。Objective： To explore the involvement of inflammasome complex on rat arterial calcification. Methods： Rats were treated with vitamin D3 300 000 U/（kg.d） compared with vehicle treated control group. HE stainning was used to evaluate the level of arterial calcification in vivo. Semi-quantitive PCR was used to detect the expression levels of NALP3, Caspase-1 and ASC. Results： The levels of NALP3, Caspase-1 and ASC were increased in the arteries of rats treated with vitamin D3 compared with vehicle treated control group. Conclusion： We build an animal model, which developed artery calcification successfully. In the process of artery calcification, NALP3 inflammasome was activated. These results provide us a platform to study the mechanism involving in artery calcification and explore new target for the therapy of artery calcification.

关 键 词：大鼠动脉钙化模型 动脉钙化 NALP3炎症小体复合物 

分 类 号：Q25[生物学—细胞生物学]