CAJ | 학술논문

目的:研究多胺在L-精氨酸抑制病理性心肌肥厚中的作用及机制.方法:异丙肾上腺素(ISO)皮下注射复制大鼠心肌肥厚模型,L-精氨酸作为干预因素,检测心脏肥大指数,心肌组织胶原染色,心房利钠肽(ANP)的转录水平,观察L-精氨酸对心肌肥大的影响;不同时段,应用高效液相色谱仪(HPLC)测定心肌组织内多胺含量,应用Western blotting结合图像分析系统,检测各组大鼠心肌组织鸟氨酸脱羧酶(ODC)和精眯/精胺乙酰转移酶(SSAT)的蛋白表达水平;检测血清NO含量和NOS活性.结果:皮下注射ISO7d后,心肌肥大指数增加,心肌纤维增粗、排列紊乱,ANP mRNA表达增加;L-精氨酸干预可抑制ISO诱导的心肌肥大,随着L-精氨酸作用时间延长,心肌组织多胺含量减少,血清NOS活性增强,NO含量增加.同时,ODC蛋白表达下调,SSAT蛋白表达上调.结论:L-精氨酸抑制ISO诱导的心肌肥大,其机制可能与下调L-精氨酸/多胺通路、上调L-精氨酸/NO通路有关.
목적:연구다알재L-정안산억제병이성심기비후중적작용급궤제.방법:이병신상선소(ISO)피하주사복제대서심기비후모형,L-정안산작위간예인소,검측심장비대지수,심기조직효원염색,심방리납태(ANP)적전록수평,관찰L-정안산대심기비대적영향;불동시단,응용고효액상색보의(HPLC)측정심기조직내다알함량,응용Western blotting결합도상분석계통,검측각조대서심기조직조안산탈최매(ODC)화정미/정알을선전이매(SSAT)적단백표체수평;검측혈청NO함량화NOS활성.결과:피하주사ISO7d후,심기비대지수증가,심기섬유증조、배렬문란,ANP mRNA표체증가;L-정안산간예가억제ISO유도적심기비대,수착L-정안산작용시간연장,심기조직다알함량감소,혈청NOS활성증강,NO함량증가.동시,ODC단백표체하조,SSAT단백표체상조.결론:L-정안산억제ISO유도적심기비대,기궤제가능여하조L-정안산/다알통로、상조L-정안산/NO통로유관.
AIM: To explore the role and possible mechanism of polyamine in L - arginine inhibiting cardiac hypertrophy induced by isoproterenol (ISO). METHODS: Hypertrophic model of rats was established using ISO. Pretrea-ted with L - arginine, hypertrophy status of rats was determined by hypertrophy coefficient, collagen content and the expression of ANP mRNA. High performance liquid chromatography ( HPLC) was used to measure the concentrations of polyamines. Western blotting was performed to detect the expressions of ornithine decarboxylase ( ODC) and spermidine/ spermine Nl - acetyltransferase (SSAT). The activity and levels of NOS and NO in serum were also observed. RESULTS : Hypertrophy coefficient and expression of ANP mRNA increased significantly after injection of ISO for 7 d. Moreover, cardiac muscle fibres became thick and disorganized. Pretreated with L - arginine, the above index decreased. Meanwhile , the concentration of polyamine was decreased and plasma NO content and NOS activity were increased, the expression of ODC was downregulated and the expression of SSAT was upregulated. CONCLUSION: Exogenous L - arginine inhibits cardiac hypertrophy through downregulating L - arginine/polyamine pathway and upregulating L - arginine/NO pathway.