FKBP12.6对异丙肾上腺素所致心脏肥大和纤维化的影响

Effects of FKBP12.6 on Cardiac Hypertrophy and Fibrosis Induced by Isoproterenol

[目的]利用FKBP结合蛋白12.6心脏特异性转基因(TG)小鼠,探讨FKBP12.6过表达在ISO所致心脏肥大纤维化病理过程中可能的保护作用。[方法]TG和对照非转基因(NTG)小鼠,连续皮下注射小剂量异丙肾上腺素(ISO),诱导扩张性心肌肥大和纤维化,通过心脏超声、PV-Loop等生理学和病理组织学等手段检测心脏功能和组织结构的变化。[结果]ISO未处理的TG和NTG小鼠相比较,心脏超声和PV-Loop指标以及纤维化和心肌细胞横截面积等无统计学差异;ISO处理后动物心脏呈扩张性肥大和纤维化表现,但TG和NTG小鼠之间功能学及病理组织学指标无统计学差异。[结论]未观察到心脏特异性过表达FKBP12.6对ISO诱导心肌损伤有明显的保护作用,FKBP12.6可能并不直接影响心肌细胞内质网RyR2的功能。

[ Objective ] FKBP binding protein 12.6TG mice was used, the protection effects of cardiac hypertrophy and fibrosis induced by FKBP12.6 over-expressed ISO were discussed. [ Method] TG and non-gene transgenic （NTG） mice were injected subcutaneously with ISO （5 mg/kg） induced cardiac hypertrophy and fibrosis, the changes of cardiac functions and organization structure were measured by cardiac ultrasound and PV-Laop of physiology and pathological tissues and so on means. [ Result] Compared with the normal NTG mice, there were no any differences in echoeardiography, PV-Loop, fibrosis and size of cardiomyoeytes in TG mice. After ISO administration, all animals showed obviously cardiac hypertrophy and fibrosis, however, there were no any statistical significance presented in the echoeardiographic, PV-Loop and morphological parameters between NTG and TG mice. [ Conclusion] There was no significant cytoprotection against cardiac injury induced by ISO. The results showed that of FKBP12.6 might not regulate the functions of RyR2 directly.