CAJ | 학술논문

目的：研究促红细胞生成素类似结构[促红细胞生成素B螺旋结构表面缩氨酸(pHBP)]对大鼠心肌缺血再灌注(I/R)损伤的影响及蛋白激酶丝氨酸/苏氨酸激酶(p44/p42 MAPK)表达。方法80只大鼠随机分为四组：假手术组(n=20)、I/R组(n=20)、I/R+促红细胞生成素(rhEPO)组(n=20)和I/R+pHBP组(n=20)。采用垫扎球囊结扎冠状动脉方法制作心肌缺血再灌注动物模型，I/R+ rhEPO组和I/R+pHBP组分别于缺血再灌注后5 min经尾静脉注射rhEPO (3000 U/kg)、pHBP (1μg/kg)，I/R组及假手术组给予等体积生理盐水，检测血清乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)含量，采用TTC染色确定梗死面积。术后3、24 h，Western blot法检测细胞外信号调节的p44/p42 MAPK表达。结果与I/R组心肌梗死面积[(18.45±1.24)%]比较，I/R+rhEPO组[(12.32±1.27)%]、I/R+pHBP组[(11.64±2.32)%]心肌梗死面积下降，差异有统计学意义(P <0.05)；与 I/R组血清 LDH [(3012.24±175.21)U/L]及CK-MB[(216.02±15.24)U/L]比较，I/R+rhEPO组和I/R+pHBP组的血清LDH及CK-MB [(2433.24±116.32)、(2511.12±98.72)、(128.16±17.52)、(121.31±21.43)U/L]均下降，差异有统计学意义(P<0.05)；制模3 h，与I/R组比较，I/R+pHBP组p44/42 MAPK蛋白表达明显增高，差异有统计学意义(P<0.05)；制模24 h，与I/R组比较，I/R+rhEPO组p44/42 MAPK蛋白表达明显增加，差异有统计学意义(P>0.05)。结论 pHBP在大鼠心肌缺血损伤中具有心脏保护作用，其保护机制可能与其抑制心肌细胞凋亡有关。
목적：연구촉홍세포생성소유사결구[촉홍세포생성소B라선결구표면축안산(pHBP)]대대서심기결혈재관주(I/R)손상적영향급단백격매사안산/소안산격매(p44/p42 MAPK)표체。방법80지대서수궤분위사조：가수술조(n=20)、I/R조(n=20)、I/R+촉홍세포생성소(rhEPO)조(n=20)화I/R+pHBP조(n=20)。채용점찰구낭결찰관상동맥방법제작심기결혈재관주동물모형，I/R+ rhEPO조화I/R+pHBP조분별우결혈재관주후5 min경미정맥주사rhEPO (3000 U/kg)、pHBP (1μg/kg)，I/R조급가수술조급여등체적생리염수，검측혈청유산탈경매(LDH)、기산격매동공매(CK-MB)함량，채용TTC염색학정경사면적。술후3、24 h，Western blot법검측세포외신호조절적p44/p42 MAPK표체。결과여I/R조심기경사면적[(18.45±1.24)%]비교，I/R+rhEPO조[(12.32±1.27)%]、I/R+pHBP조[(11.64±2.32)%]심기경사면적하강，차이유통계학의의(P <0.05)；여 I/R조혈청 LDH [(3012.24±175.21)U/L]급CK-MB[(216.02±15.24)U/L]비교，I/R+rhEPO조화I/R+pHBP조적혈청LDH급CK-MB [(2433.24±116.32)、(2511.12±98.72)、(128.16±17.52)、(121.31±21.43)U/L]균하강，차이유통계학의의(P<0.05)；제모3 h，여I/R조비교，I/R+pHBP조p44/42 MAPK단백표체명현증고，차이유통계학의의(P<0.05)；제모24 h，여I/R조비교，I/R+rhEPO조p44/42 MAPK단백표체명현증가，차이유통계학의의(P>0.05)。결론 pHBP재대서심기결혈손상중구유심장보호작용，기보호궤제가능여기억제심기세포조망유관。
Objective To investigate the protective effects of small nonerythropoietic helix B surface peptide (pHBP) based upon erythropoietin structure on heart ischemic myocardial damage (I/R) of rats, and the expression effect of p44/p42 MAPK. Methods 40 rats were randomly divided into 4 groups:sham-operated group (n=10), I/R group (n=10), I/R+rhE-PO group (n=10) and I/R+pHBP group (n=10). Experimental model was established by ligating the left anterior descend-ing coronary artery, I/R+rhEPO group and I/R+pHBP group were treated with rhEPO (3000 U/kg), pHBP (1 μg/kg) re-spectively after ischemia reperfusion 5 min, and the sham operation group and I/R group were given saline instead. Serum LDH,CK-MB were assessed, myocardial infarct areas were measured by TCC dyeing. After 3, 24 h of treatment, the expression of p44/p42 MAPK was analysized through Westen blot. Results he myocardial infarct size of I/R+rhEPO group [(12.32±1.27)%] and I/R+pHBP group [(11.64±2.32)%] were decreased than that of I/R group [(18.45±1.24)%], the differences were statistically significant (P < 0.05); the content of LDH and CK-MB in I/R+rhEPO group [(3012.24±175.21), (216.02±15.24) U/L] and I/R+pHBP group [(2433.24±116.32), (2511.12±98.72), (128.16±17.52), (121.31±21.43) U/L] were decreased than those of I/R group, the differences were statistically significant (P< 0.05), Compared with I/R group, the expression of p44/42 MAPK in I/R+pHBP group and I/R+rhEPO group were increased at model made 3 hours and 24 hours respectively, the differences were statistically significant (P < 0.05). Conclusion pHBP has a cadioprotective effect on heart ischemic damage. The protective mechanism may be related to the function of inhibition of myocardial cell apoptosis.