CAJ | 학술논문

目的：探讨缺氧预处理（H PC ）对于心肌钙网蛋白表达与肌浆网钙稳态的影响及其信号转导机制。方法选择SD大鼠22只，随机分为假手术组6只，模型组8只，H PC组8只。复制SD大鼠H PC和心肌梗死模型，检测左心室压力最大上升速率和最大下降速率（± dp/dtmax ）、T TC法测定心肌梗死面积，差速离心法制备心肌肌浆网并鉴定其纯度，以Millipore滤过法测定肌浆网Ca2＋摄取活性和肌浆网Ca2＋释放速率，Western blot检测钙网蛋白、p38丝裂原活化蛋白激酶和磷酸化 p38丝裂原活化蛋白激酶水平。结果与假手术组比较，模型组＋ dp/dtmax和-dp/dtmax分别下降39％和46％（P＜0．05）；与模型组比较，HPC组分别升高43％和59％（P＜0．05），肌浆网Ca2＋摄取升高[（60．38±5．76）nmol Ca2＋/（mg?min） vs （31．10±3．13）nmol Ca2＋/（mg?min）]，肌浆网Ca2＋释放降低[（32．12±1．18）nmol Ca2＋/（mg?15 s） vs （39．61±1．16）nmol Ca2＋/（mg?15 s），P＜0．05]，钙网蛋白表达和p38丝裂原活化蛋白激酶水平明显升高（ P＜0．05）。结论 H PC通过p38丝裂原活化蛋白激酶途径上调钙网蛋白表达，改善心肌肌浆网C a2＋摄取和肌浆网C a2＋释放功能、减轻细胞内钙超载而保护缺血心肌。
목적：탐토결양예처리（H PC ）대우심기개망단백표체여기장망개은태적영향급기신호전도궤제。방법선택SD대서22지，수궤분위가수술조6지，모형조8지，H PC조8지。복제SD대서H PC화심기경사모형，검측좌심실압력최대상승속솔화최대하강속솔（± dp/dtmax ）、T TC법측정심기경사면적，차속리심법제비심기기장망병감정기순도，이Millipore려과법측정기장망Ca2＋섭취활성화기장망Ca2＋석방속솔，Western blot검측개망단백、p38사렬원활화단백격매화린산화 p38사렬원활화단백격매수평。결과여가수술조비교，모형조＋ dp/dtmax화-dp/dtmax분별하강39％화46％（P＜0．05）；여모형조비교，HPC조분별승고43％화59％（P＜0．05），기장망Ca2＋섭취승고[（60．38±5．76）nmol Ca2＋/（mg?min） vs （31．10±3．13）nmol Ca2＋/（mg?min）]，기장망Ca2＋석방강저[（32．12±1．18）nmol Ca2＋/（mg?15 s） vs （39．61±1．16）nmol Ca2＋/（mg?15 s），P＜0．05]，개망단백표체화p38사렬원활화단백격매수평명현승고（ P＜0．05）。결론 H PC통과p38사렬원활화단백격매도경상조개망단백표체，개선심기기장망C a2＋섭취화기장망C a2＋석방공능、감경세포내개초재이보호결혈심기。
Objective To study the effect of hypoxic preconditioning (HPC) on myocardial calreti-culin (CRT ) expression and calcium homeostasis in sarcoplasmic reticulum (SR) and its signal transduction mechanism .Methods Twenty-two SD rats were randomly divided into sham opera-tion group(n=6) ,model group (n=8) ,and HPC group (n=8) .SD rat HPC model and myocardial infarction (MI) model were established .The LV ± dp/dtmax was assayed .The infarction size was measured by TTC .The SR vesicle was prepared and its purity was identified by differential cen-trifugation .The SR Ca2+ uptake and release were detected by Millipore filtration .CRT expression and p38MAPK phosphorylation were detected by Western blot .Results The LV + dp/dt max and -dp/dtmax were 39% and 46% lower in HPC group than in sham operation group (P<0 .05) , and 43% and 59% higher in HPC group than in model group (P<0 .05) .The SR Ca2+ uptake was higher and the SR Ca2+ release was lower in HPC group than in model group (P<0 .05) .The CRT expression and p38MAPK phosphorylation levels were higher in HPC group than in model group (P<0 .05) .Conclusion HPC can upregulate the Ca2+ expression ,improve the SR Ca2+ up-take and release ,and reduce the calcium overload in myocardiocytes through the p38MAPK path-way ,thus protecting the heart against ischemia injury .