CAJ | 학술논문

目的：观察乌司他丁对心肌缺血再灌注后大鼠心肌细胞的保护机制。方法采用垫扎球囊法结扎冠状动脉制作心肌缺血再灌注的动物模型，30只大鼠随机分为三组：假手术组(n=10)、缺血/再灌注(I/R)组(n=10)和I/R+乌司他丁组(n=10)。检测三组心肌组织谷胱甘肽(GSH)、丙二醛(MDA)及血清标志物肌酸激酶同工酶(CK-MB)含量，采用TTC染色确定心肌梗死及缺血范围，并用Western-blot测定炎症因子白细胞介素-6(IL-6)、IL-8的表达。结果与假手术组比较，I/R组中反映氧化损伤程度的MDA明显升高[(4.13±3.27)nmol/L比(11.13±2.13)nmol/L]，CK-MB也升高[(15.21±6.24)U/L比(2752.21±1276.36)U/L]，GSH则明显降低[(241.42±3.28)mg/L比(184.26±2.14)mg/L]，差异均有高度统计学意义(P<0.01)；与I/R组比较，I/R+乌司他丁组MDA[(8.25±4.26)nmol/L]、CK-MB[(1873.24±621.43)U/L]含量降低，差异有统计学意义(P<0.05)。I/R+乌司他丁组梗死面积[(12.27±4.26)%]小于I/R组[(17.12±3.18)%]，差异有统计学意义(P<0.05)。假手术组IL-6、IL-8水平较低[(0.412±0.550)、(0.132±0.071)]，缺血再灌注后，I/R组IL-6、IL-8表达升高[(1.785±0.720)、(0.926±0.247)]，差异有高度统计学意义(P<0.01)；与I/R组比较，I/R+乌司他丁组炎性因子IL-6、IL-8水平下降[(1.102±0.780)、(0.672±0.240)]，差异有统计学意义(P<0.05)。结论乌司他丁具有抗心肌缺血再灌注损伤作用，其机制可能是通过下调IL-6和IL-8介导的炎性反应而实现。
목적：관찰오사타정대심기결혈재관주후대서심기세포적보호궤제。방법채용점찰구낭법결찰관상동맥제작심기결혈재관주적동물모형，30지대서수궤분위삼조：가수술조(n=10)、결혈/재관주(I/R)조(n=10)화I/R+오사타정조(n=10)。검측삼조심기조직곡광감태(GSH)、병이철(MDA)급혈청표지물기산격매동공매(CK-MB)함량，채용TTC염색학정심기경사급결혈범위，병용Western-blot측정염증인자백세포개소-6(IL-6)、IL-8적표체。결과여가수술조비교，I/R조중반영양화손상정도적MDA명현승고[(4.13±3.27)nmol/L비(11.13±2.13)nmol/L]，CK-MB야승고[(15.21±6.24)U/L비(2752.21±1276.36)U/L]，GSH칙명현강저[(241.42±3.28)mg/L비(184.26±2.14)mg/L]，차이균유고도통계학의의(P<0.01)；여I/R조비교，I/R+오사타정조MDA[(8.25±4.26)nmol/L]、CK-MB[(1873.24±621.43)U/L]함량강저，차이유통계학의의(P<0.05)。I/R+오사타정조경사면적[(12.27±4.26)%]소우I/R조[(17.12±3.18)%]，차이유통계학의의(P<0.05)。가수술조IL-6、IL-8수평교저[(0.412±0.550)、(0.132±0.071)]，결혈재관주후，I/R조IL-6、IL-8표체승고[(1.785±0.720)、(0.926±0.247)]，차이유고도통계학의의(P<0.01)；여I/R조비교，I/R+오사타정조염성인자IL-6、IL-8수평하강[(1.102±0.780)、(0.672±0.240)]，차이유통계학의의(P<0.05)。결론오사타정구유항심기결혈재관주손상작용，기궤제가능시통과하조IL-6화IL-8개도적염성반응이실현。
Objective To observe the protection mechanism of Ulinastain on heart ischemia/reperfusion injury in rats. Methods Experimental model was established by ligation of coronary artery with PTCA balloon, 30 Wistar rats were randomly divided into three groups: sham operation group (n=10); ischemia/reperfusion (I/R) group (n=10); I/R+Ulinas-tain group (n=10). The GSH and MDA of cardiac muscle tissues, and the serum biomarkers CK-MB in three groups were detected; ischemic and infarct areas in three groups were measured by TCC dyeing; the expression of IL-6 and IL-8 were analyzed by Western-blot analysis. Results Compared with sham operation group, the level of MDA which reflect the degree of oxidative damage in I/R group increased significantly [(4.13±3.27)nmol/L vs(11.13±2.13)nmol/L], and the CK-MB was increased [(15.21±6.24)U/L vs(2752.21±1276.36)U/L], the value of GSH was decreased signifi-cantly, the differences were statistically significant (P<0.01);compared with I/R group, MDA of I/R+Ulinastain group [(8.25±4.26)nmol/L], CK-MB [(1873. 24±621.43)U/L] decreased, the differences were statistically significant (P<0.05). Infarction area of I/R+Ulinastain group [(12.27±4.26)%] was lower than that of I/R group [(17.12±3.18)%], the difference was statistically significant(P<0.05); the levels of IL-6 and IL-8 in sham operation group [(0.412±0.550), (0.132±0.071)] were lower, after ischemia reperfusion, the levels of IL-6 and IL-8 in I/R group [(1.785±0.720), (0.926±0.247)] was increased, the differences were statistically significant (P<0.01);compared with I/R group, the level of IL-6 and IL-8 in I/R+Ulinastain group [(1.102±0.780), (0.672±0.240)] was decreased, the differences were statistically sig-nificant (P<0.05). Conclusion Ulinastain may protect myocardium from ischemia reperfusion injury by modulating the expression of IL-6 and IL-8 proteins and inhibiting inflammation.