姜黄素抑制尾加压素-Ⅱ诱导的人晶状体上皮细胞增殖及[Ca^(2+)]_i、cAMP、cGMP信号转导机制  

Effect of Curcumin on proliferation inhibition induced by Urotensin-Ⅱ in human lens epithelial cell and its mechanism of signal transduction

作　　者：祁明信[1] 黄秀榕[2] 胡俊[2] 杨丽英[2] 

机构地区：[1]福建中医学院附属第二人民医院眼科 [2]福建中医学院病理生理研究中心

出　　处：《中国临床药理学与治疗学》2009年第10期1085-1090,共6页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：福建省中医药重点项目(Wzzb0601)

摘　　要：目的:探讨姜黄素(curcumin,Cur)抑制尾加压素II(urotensinⅡ,U-II)诱导的人晶状体上皮细胞(human lens epithelial cell,HLEC)增殖及[Ca2+]i、cAMP、cGMP信号转导机制。方法:将U-II诱导体外培养的HLEC发生增殖,并用不同浓度的Cur与其共同孵育后,用MTT法检测HLEC的活性;用流式细胞术(flowcytometer,FCM)检测HLEC增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)表达;用荧光分光光度法检测HLEC内游离钙离子浓度[Ca2+]i;用放射免疫分析法检测HLEC内环化腺苷酸(cyclic adenosine monophos-phate,cAMP)和环化鸟苷酸(cyclic guanosine mono-phosphate,cGMP)浓度。结果:U-II组HLEC活性、PCNA蛋白表达和cGMP浓度均高于对照组(P<0.01);Cur组HLEC活性、PCNA蛋白表达和cGMP浓度均比U-II组降低(P<0.01)。U-II组HLEC[Ca2+]i比对照组显著升高(P<0.01),U-II组cAMP浓度比对照组显著降低(P<0.01);Cur组与U-II组比较[Ca2+]i、cAMP浓度显著升高(P<0.01)。结论:Cur可抑制U-II诱导的HLEC增殖。[Ca2+]、cAMP-PKA、cGMP-PKG是其重要的细胞信号转导机制。Cur有可能成为防治后发性白内障的有效药物。AIM：To study the effect of Curcumin（Cur）on proliferation inhibition induced by urotensin-Ⅱ in human lens epithelial cell （HLEC） and its signal transduction mechanism of [Ca^2＋]i,cAMP and cGMP.METHODS：The cultured HLEC were incubated with different concentrations of Cur and the HLEC activities were detected via MTT assay.The proliferative cell nuclear antigen （PCNA）of HLEC were detected via flow cytometer（FCM）.The concentration of intracellular free calcium （[Ca^2＋]i） of HLEC were determined by spectrofluoremeter.The intracellular contents of cyclic adenosine monophosphate （cAMP） and cyclic guanosine monophosphate （cGMP） of HLEC were detected by radioimmunoassay.RESULTS：The activity,expression of PCNA and the cGMP concentration of HLEC in U-Ⅱ group were higher than those in control group,but they were significantly decreased in Cur group （P〈0.01）.Compared with control group,the [Ca^2＋]i concentration of HLEC in U-Ⅱ group was increased,and the cAMP concentration in U-Ⅱ group was decreased（P〈0.01）.Compared with U-Ⅱ group,the concentrations of cAMP and [Ca^2＋]i were increased （P〈0.01）.CONCLUSION：Cur can inhibit the proliferation of HLEC induced by urotensin-Ⅱ.The signal transduction of [Ca^2＋],cAMP-PKA and cGMP-PKG may play an important role in it.Cur may become an effective drug of preventing and treating after-cataract.

关 键 词：尾加压素Ⅱ 姜黄素 晶状体上皮细胞 增殖 信号转导 后发性白内障 

分 类 号：R965.2[医药卫生—药理学]