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作 者:洪乐鹏[1] 邵帅[1] 谭珍[2] 甘斯婷 汪光亮[3]
机构地区:[1]广州医科大学人体解剖教研室,511436 [2]广州医科大学第一临床学院,511436 [3]广州医科大学组胚教研室,511436
出 处:《中国临床神经科学》2016年第3期260-266,共7页Chinese Journal of Clinical Neurosciences
基 金:广东省科学技术厅资助项目(编号:201301);广东省医学科研基金厅资助项目(编号:A2013239)
摘 要:目的探讨2,6,9-三取代嘌呤化合物(PM)激活BV2细胞中SHH信号通路发挥抑制炎症作用的分子机制。方法 BV2细胞按实验需要分为1对照组;2脂多糖(LPS)组;3PM+LPS组;4PM组。PM激活BV2细胞中SHH信号通路后,应用荧光定量PCR(Q-PCR)检测Smad6、E3泛素连接酶Peli1、炎症转录因子(NF-κB)以及转化生长因子β1(TGF-β1)的m RNA表达情况。结果与对照组比较,LPS刺激后Smad6 m RNA表达下降(P<0.01),Peli1 m RNA和NF-κB m RNA表达升高(均P<0.01),PM处理后能促进Smad6 m RNA和TGF-β1 m RNA表达(P<0.01,P<0.05);与LPS组比较,PM对LPS作用下的Peli1 m RNA和NF-κB m RNA表达起抑制作用(均P<0.01)。结论 PM激活SHH信号通路后发挥抗炎作用下调Peli1和NF-κB表达水平,可能与上调Smad6表达和增加TGF-β1表达水平有关。Aim To investigate the molecular mechanism of inhibiting inflammation through sonic hedgehog(SHH) signaaling pathway activated by purmorphamine(PM)in BV2 cells.Methods The BV2 cells were divided into a control group,a lipopolysaccharide(LPS) group,a PM+LPS group and a PM group.After PM activating SHH signaling pathway in BV2 cells,real-time Quantitative PCR(Q-PCR) was used to detect the expression of Smad6,E3 ubiquitin ligase Peli1,inflammatory transcription factor NF-κB and transforming growth factor(TGF-β1) m RNA.Results Compared with the control group,the expression of Smad6 m RNA decreased(P0.01) and Peli1,NF-κB m RNA increased(all P0.01) after LPS stimulation,PM treatment could promote Smad6 and anti-inflammatory cytokine TGF-β1 m RNA expression(P0.01,P0.05);Compared with the LPS group,PM could inhibite the expression of Peli1 and NF-κB m RNA after LPS stimulation(all P0.01).Conclusion PM plays a role of inhibiting inflammation byinhibiting the expression of Peli1 and NF-κB through activating SHH signaling pathway,which may be related to increasing the expression of Smad6 and TGF-β1.
关 键 词:2 6 9-三取代嘌呤化合物 SHH信号通路 SMAD6 炎症 脂多糖
分 类 号:R741.05[医药卫生—神经病学与精神病学]
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