摘要
目的动态观察血小板数(Plt)、血小板生成素(TPO)、转化生长因子β1(TGF-β1)在幼兔免疫性血管炎模型中的变化,探讨Plt、TPO、TGF-β1在川崎病(KD)发病过程中的作用及相关性。方法用牛血清白蛋白复制幼兔免疫性血管炎的KD动物模型,50只幼兔分为实验组25只和对照组25只,每隔4 d分别检测Plt、TPO水平、TGF-β1阳性率和积分值,并于第17、28天取冠状动脉、肝、脾、肾、脑等组织作病理学分析。结果Plt于第12、16、20、24、28天在实验组较对照组明显升高,差异有显著性(P<0.05);TPO水平于第8、12、16、20、24、28天在实验组比对照组明显升高,差异有显著性(P<0.05);TGF-β1阳性率和积分值于第16、20、24、28天在实验组比对照组明显升高,差异有显著性(P<0.05)。Plt在实验组与TPO水平、TGF-β1阳性率及积分值均呈正相关(r分别为0.427、0.425、0.291,P<0.01);而在对照组与TPO水平呈正相关(r=0.580,P<0.05),与TGF-β1阳性率及积分值呈负相关(r=-0.288,P<0.05);实验组幼兔第17天肝、脾、肾、脑、心及冠状动脉组织病理检查可见微小动脉不同程度内皮细胞肿胀、坏死、内皮下组织水肿、血管壁炎性细胞浸润和弹力纤维断裂等改变,第28天可见中小动脉炎性损伤改变,而主动脉均仅见轻度内皮细胞肿胀。结论血小板、TPO、TGF-β1共同参与KD的病理发病机制,在KD的病理生理过程中相互作用,相互协调,提示Plt、TPO、TGF-β1均可作为监测KD病情变化的重要指标及为KD的临床诊治提供新的途径。
Objective To investigate the role of platelet count （PLT）, thrombopoietin （TPO） and transforming growth factor β1 （TGF - β1 ） in pathogenesis of Kawasaki disease and their correlation. Methods An experimental model of weanling rabbits for Kawasaki disease （KD） was established with bovine serum. There were 50 weanling rabbits, with 25 in control group and 25 in experimental group. Levels of PLT, TPO and TGF - β1 were examined every four days. Histological study of coronary artery, Liver, spleen, kidney and brain was performed. Results PLT was higher in the experimental group than that of the control group 12, 16, 20, 24, 28 days after infection （P 〈0. 05） ; TPO was higher in the experimental group than that of the control group 8, 12, 16, 20, 24, 28 days after infection. （P〈O. 05） TGF -β1 was higher in the experimental group than that of the control group 16, 20, 24, 28 days after infection （P 〈0.05 ） PLT was positively correlated with TPO and TGF-β1 （P 〈 0. 01 ） in the experimental group. In the control group, PLT was positively correlated with TPO （P 〈0. 01 ）, but negative correlated with TGF -β1 （P 〈0. 05） ; Histological study of cor- onary artery, liver, spleen, kidney and brain of showed various degree of alterations including swelling and necrosis of small artery endothelium, edema in subcutaneous tissue, inflammatory cell infiltration and elastic fibers fracture in 17 days after injection in the experimental group. Twenty - eight days after injection, inflammatory changes were observed at small and medium -sized artery, whereas only mild changes were observed in the aorta. Conclusion Platelets, TPO and TGF - β1 play critical roles in the pathogenesis of KD through their interaction. Thus PLT, TPO and TGF - β1 are potential markers for monitoring the progression of KD, providing novel strategy for clinical diagnosis and treatment.
出处
《广东医学》
CAS
CSCD
北大核心
2010年第1期32-35,共4页
Guangdong Medical Journal
基金
湖南省教育厅科研基金项目(编号:07C571)
湖南省科技厅科研基金项目(编号:089K3061)
