CAJ | 학술논문

目的通过检测血清中一氧化氮(NO)和肺组织核转录因子-κB p65(NF-κB p65)的变化,探讨阿魏酸钠(sodium ferulate,SF)对兔肺缺血再灌注损伤(I/R)的保护作用和机制.方法采用复制Sekido模式再造兔肺缺血再灌注损伤模型,将实验动物(新西兰大白兔,1.8-2.5 kg)分为3组,每组6只:假手术组(S组,只开胸分离左肺韧带而不结扎肺门),SF处理组(SF组,在行左肺I/R前10min耳缘静脉注射ST,100 mg/kg)和缺血再灌注损伤组(I/R组,开胸分离左肺韧带并结扎肺门).分别在缺血前、缺血60min、再灌注30、120 min时抽取颈动脉血液离心测定血清NO,实验结束时取肺组织行NF-κB p65免疫组化灰度值测定.结果 SF预处理保护和提高了再灌注30 min(28.650±6.185)以及再灌注120 min(33.748±6.157)内源性NO活性,与I/R组(15.070±8.560;20.500±4.619)差异有统计学意义(P<0.01);抑制了NF-κB p65(78.852±4.875)在再灌注损伤肺组织中的激活,与I/R组(63.390±1.190)差异有统计学意义(P<0.01),减轻肺组织的再灌注损伤.结论 SF预处理能够降低肺组织的缺血再灌注损伤,其机制可能是通过减低内皮舒张因子NO产生源的破坏和抑制NF-κB p65的活化,进而减轻炎症损害作用.
목적 통과검측혈청중일양화담(NO)화폐조직핵전록인자-κB p65(NF-κB p65)적변화,탐토아위산납(sodium ferulate,SF)대토폐결혈재관주손상(I/R)적보호작용화궤제.방법 채용복제Sekido모식재조토폐결혈재관주손상모형,장실험동물(신서란대백토,1.8-2.5 kg)분위3조,매조6지:가수술조(S조,지개흉분리좌폐인대이불결찰폐문),SF처리조(SF조,재행좌폐I/R전10min이연정맥주사ST,100 mg/kg)화결혈재관주손상조(I/R조,개흉분리좌폐인대병결찰폐문).분별재결혈전、결혈60min、재관주30、120 min시추취경동맥혈액리심측정혈청NO,실험결속시취폐조직행NF-κB p65면역조화회도치측정.결과 SF예처리보호화제고료재관주30 min(28.650±6.185)이급재관주120 min(33.748±6.157)내원성NO활성,여I/R조(15.070±8.560;20.500±4.619)차이유통계학의의(P<0.01);억제료NF-κB p65(78.852±4.875)재재관주손상폐조직중적격활,여I/R조(63.390±1.190)차이유통계학의의(P<0.01),감경폐조직적재관주손상.결론 SF예처리능구강저폐조직적결혈재관주손상,기궤제가능시통과감저내피서장인자NO산생원적파배화억제NF-κB p65적활화,진이감경염증손해작용.
Objective To investigate protective and effects of the sodium fendate on rabbit lung from ischemia-reperfusion inju-ry by studying serum nitric oxide (NO) and lung tissue nuclear factor-κB p65 (NF-κB p65). Methods Reproducing the Sekido mod-al of the ischemia-reperfusion in rabbit lung, 18 rabbits were divided into 3 Stoups, the sham group (n=6); ischemic-reperfusion group (n = 6 ) : the left lung hilus were clamped to ischemic and then followed by reperfusion as I/R; preconditioning group(SF, n = 6) : treated with 100 mg/kg SF before I/R ). Blood from samples were collected the common carotid at the following time points (be- fore ischemia, ischemia 60 mins, reperfused 30 mins, reperfused 120 mins), studied for NO. The lung tissues NF-κB p65 was as- sayed by immunohistochemitry. Results Sodium ferulate preconditioning increased the endogenous NO at the time points 30 mins (28.650±6.185) and 120 mins (33.748±6.157), significant different statistically from I/R group (15.070±8.560, 20.500± 4.619, P<0.01), and inhibited the NF-κB 1065 in SF group (78.852±4.875), also significantly different from the I/R group (63.390±1.190). Conclusion Sodium ferulate can protect the lung from I/R injury by decreasing the destruction of the NO and depressing the NF-κB p65 and thus abates inflammatoty lung injury.