【摘 要】
：
Objective Previous studies showed that the inhibition of proteasome activity could significantly improve cardiac hypertrophy,but its mechanism is not clear.Increased glycogen synthase kinase-3 (GSK-3)
【机 构】
：
Department of pharmacology, School of pharmaceutical sciences, Guangzhou Medical University.Xinzao,
【出 处】
：
广东省药理学会第七届2015学术交流大会
论文部分内容阅读
Objective Previous studies showed that the inhibition of proteasome activity could significantly improve cardiac hypertrophy,but its mechanism is not clear.Increased glycogen synthase kinase-3 (GSK-3) activity can also improve cardiac hypertrophy.However,the relationship between proteasome and GSK-3 has not been reported in cardiomyocyte In this study,we will investigate the effect of proteasome inhibition on cardiomyocyte hypertrophy,GSK-3 activity and the underlying mechanism.Methods Primary neonatal rat cardiomyocytes were divided into 4 groups: Control,Ang Ⅱ (100nM,48h),Ang Ⅱ (100nM) +MG132 (0.05 μM),MG132 (0.05 μM),Ang Ⅱ (100nM) +MG132+LiCl (10 mM),LiCl.Proteasomeactivitiywas detected by fluorescent peptide substrate.
其他文献
目的：研究血府逐瘀汤抗高血压心肌纤维的作用机制。方法：HPLC法建立血府逐瘀汤免煎颗粒指纹图谱；心肌成纤维细胞分离、培养与鉴定：用胰酶消化组织分离细胞,差速贴壁法纯化获得心肌成纤维细胞,用光学显微镜和免疫细胞化学的方法鉴定细胞；CCK-8法检测TGF-β1诱导后心肌成纤维细胞的增殖情况；RT-QPCR,Western-blot检测血府逐瘀汤对TGF-β1诱导后心肌成纤维细胞Ⅰ型胶原,Smad 2,
目的：研究microRNA-181a对高脂饮食诱导的apoE-/-小鼠肾损伤的保护作用.方法：将apoE-/-小鼠分为4组：Normal diet组,HFD组、HFD+NC-m组、HFD+181a-m组.5周ApoE-/-小鼠高脂饮食或正常饮食12周后,NC-m组尾静脉注射negative control mimics,181a-m组尾静脉注射miR-181a-mimics(50μg/kg/w),
[Objectives]To establish the rat model of secondary osteoporosis in rheumatoid arthritis (RA) and investigate the characteristics of RA to induce osteoporosis in the course of disease development.At t
目的：前期研究发现，自噬在急性心肌梗死后早期被迅速激活，但自噬底物P62随缺血时间延长发生堆积，提示自噬流在心肌持续缺血后受损。本研究旨在探讨损伤调节自噬调控基因1(DRAM1)是否能够通过改善自噬流抗心肌细胞缺血损伤。
Aims: Previous study from our lab reported that sonic hedgehog (Shh) pathway plays a protective role in myocardial infarction (MI) through against the damage of cardiomyocytes,but the underlying mecha