摘要
目的:探讨特发性血小板减少性紫癜(ITP)模型小鼠体内,过氧化物酶体增生物激活受体γ(PPAR-γ)对一氧化氮(NO)生成的影响及意义。方法:ITP模型小鼠分成罗格列酮试验组、GW9662对照组和磷酸盐缓冲液(PBS)对照组,罗格列酮试验组用相同浓度(20μmol/L)的PPAR-γ激活剂噻唑烷二酮(thiazolidinediones,TZD)类药物罗格列酮进行灌肠,同时设立的GW9662对照组:使用PPAR-γ特异性拮抗剂GW9662的终浓度为10μmol/L,PBS对照组使用相同体积的磷酸盐缓冲液进行灌肠,用药6、12、18、24和30小时后,用硝酸还原酶法检测小鼠血液NO含量,RT-PCR法检测血液淋巴细胞PPAR-γmRNA表达情况。结果:血清中NO在第6、12、18、24和30小时的含量罗格列酮试验组高于GW9662对照组及PBS对照组(均P<0.05)。在罗格列酮试验组中,NO含量随着用药时间的延长而升高,各测量时间点NO含量具有统计学差异(P<0.05),PPAR-γmRNA的表达随着时间的延长而增加(P<0.05),NO表达量与PPAR-γ的表达呈正相关(r=0.89,P<0.05)。结论:在ITP小鼠模型内,PPAR-γ活化剂能够以时间依赖的形式增加NO的生成,PPAR-γ可能通过NO途径来发挥相应的生理功能。
Objective：To investigate the influence and significance of PPAR-γ on nitric oxide （NO） production in ITP model mice.Methods：ITP model mice were divided into rosiglitazone experimental group,GW9662 control group and phosphate buffered saline （PBS） control group.The mice of rosiglitazone experimental group was given with the same concentration （20 μmol/L） of the PPAR-γ activator rosiglitazone of Thiazolidine drug by enema,and at the same time,GW9662 control group as established by the use of PPAR-γ antagonist GW9662 with the final concentration of 10 μmol/L,PBS control group as established by the same volume of phosphate buffer at 6 h,12 h,18 h,24 h and 30 h after the usage of drug.NO content in blood of the mice was detected by nitrate reductase,and the expression of PPAR-γ mRNA in blood lymphocytes was tesed by RT-PCR.Results：The serum NO amount of rosiglitazone experimental group was higher than in the GW9662 control group and PBS control group in the form of serum NO content in the first 6 h,12 h,18 h,24 h and 30 h （all P0.05）.In rosiglitazone experimental group,NO concentration increased with the duration of drug usage,NO content was shown the significant differences at all the measurement time points （P0.05）,PPAR-γ mRNA expression increased with the time （P0.05）,and NO content and the expression of PPAR-γ were positively correlated （r=0.89,P0.05）.Conclusion：PPAR-γ activator is able to increase NO production relying on the time of drug usage and PPAR-γ might adjust the target factors by NO pathway in ITP model mice.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2010年第7期591-594,共4页
Chinese Journal of Immunology
基金
广东省自然科学基金(No.06028959)
广东省东莞市科技计划项目(No.2008108101033)
广东医学院青年基金(No.XQ06017)
