体内
颈静脉
基因表达
体外
化学
RNA干扰
信使核糖核酸
药理学
生物
NF-κB
实时聚合酶链反应
小干扰RNA
基因沉默
医学
分子生物学
基因
内科学
细胞生物学
信号转导
内分泌学
核糖核酸
生物化学
生物技术
作者
W Ye,X Ten,Mingming He,Yanhui Yu,Haohai Huang,Yingbin Hu,Chen Y,Xinke Zhou,Zhenya Shen
出处
期刊:Methods and Findings in Experimental and Clinical Pharmacology
[Thomson Reuters (Prous Science)]
日期:2010-01-01
卷期号:32 (6): 391-391
被引量:7
标识
DOI:10.1358/mf.2010.32.6.1472186
摘要
The nuclear factor-kappaB (NF-κB) in cardiac vascular endothelial cells (type II VEC) is a key factor that activates delayed xenograft rejection (DXR), and therefore inhibition of NF-κB gene expression may alleviate post-transplant rejection. siRNA technology was used to inhibit NF-κB p65 gene expression in ICR mice. After jugular vein injection of siRNA/in vivo-jetPEI complex, fluorescence levels of FAM-labeled siRNA in hearts and lungs were much higher after jugular vein injection than tail vein injection, suggesting more efficient siRNA delivery to the heart through the jugular vein. The amount of FAM fluorescence of hearts increased to the highest level between 48 and 72 hours after injection, and decreased gradually 1 week after injection. A minimum dose of 6 nmol NF-κB p65 siRNA and a siRNA/in vivo-jetPEI ratio of 6 (N/P = 6) were required for in vivo siRNA-mediated gene silencing in the heart. Under these conditions, application of siRNA/in vivo-jetPEI complexes from the jugular vein successfully suppressed NF-κB p65 expression in the heart. The same strategy can be applied to heart transplant animal models to protect against NF-κB gene-related type II VEC activation and xenograft rejection.
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