论文部分内容阅读
目的探讨在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)对一氧化氮合酶(NOS)生成的影响。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(20umol/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30h后,检测小鼠血清中NOS活性和血液淋巴细胞PPAR-γmRNA表达情况。结果血清中NOS在第6,12,18,24和30h的活性,罗格列酮试验组高于GW9662对照组及PBS对照组(P均<0.05)。在罗格列酮试验组中,NOS活性随着用药时间的延长而升高,各测量时间点NOS活性具有统计学差异(P<0.05),PPAR-γmRNA的表达随着时间的延长而增加(P<0.05),PPAR-γ的表达与NOS活性呈正相关(r=0.82,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NOS的活性,PPAR-γ可能通过NOS途径来发挥相应的生理功能。
Objective To investigate the effect of PPAR-γ on nitric oxide synthase (NOS) production in idiopathic thrombocytopenic purpura (ITP) model mice. Methods The ITP mice were divided into rosiglitazone group, GW9662 control group and phosphate buffered saline (PBS) control group. The rosiglitazone group was treated with PPAR-γ activator thiazolidine di The thiazolidinediones (TZD) -like drug rosiglitazone was used in the enema. At the same time, the GW9662 control group was established with the PPAR-γ specific antagonist GW9662 at a final concentration of 10 μmol / L, and the PBS control group was treated with the same volume of phosphate buffer After 6, 12, 18, 24 and 30 hours, the NOS activity in serum and the expression of PPAR-γmRNA in blood lymphocytes were detected. Results Serum NOS activity at 6th, 12th, 18th, 24th and 30th hour in rosiglitazone test group was higher than that in GW9662 control group and PBS control group (all P <0.05). In the rosiglitazone group, the activity of NOS increased with the prolongation of administration time, the activity of NOS at each time point was statistically different (P <0.05), and the expression of PPAR-γ mRNA increased with time ( P <0.05). There was a positive correlation between the expression of PPAR-γ and NOS activity (r = 0.82, P <0.05). Conclusion In ITP mouse model, PPAR-γ activator can increase the activity of NOS in a time-dependent manner. PPAR-γ may exert corresponding physiological functions through NOS pathway.