摘要
目的:观察莱菔硫烷(sulforaphane,SFN)对大鼠移植心脏冷缺血再灌注损伤的影响。方法:健康雄性Lewis大鼠60只随机分成3组,每组20只。对照组:受体大鼠于移植前24 h经鼠尾静脉注射等量的生理盐水;NAC组:受体大鼠于移植前半小时经下腔静脉注射N-乙酰半胱氨酸(N-acetylcysteine,NAC)300 mg/kg;SFN组:受体大鼠于移植前24 h经尾静脉注射SFN 2.5 mg/kg。其中供心冷藏于4℃HTK液18 h,建立大鼠心脏移植模型。采用半定量法评价心脏功能,再灌注后6、24 h分别从受体鼠内眦静脉和下腔静脉取血,检测血清中乳酸脱氢酶(lactate dehydrogenase,LDH)、肌酸激酶同工酶(creatinekinase-MB,CK-MB)、肌钙蛋白(troponin T,TnT)的水平;移植后24 h摘取供心,观察心肌组织学及超微结构的变化,检测心肌组织中超氧化物歧化酶(superoxide dismutase,SOD)的活性及脂质过氧化物(lipid hydroperoxide,LPO)含量。结果:心脏功能评分SFN组、NAC组较对照组均明显提高(P<0.05);再灌注6 h,与对照组相比,NAC组血清中LDH、CK-MB和TnT的活性均降低(P<0.05)。SFN组血清中LDH、CK-MB和TnT的活性均降低(P<0.05);再灌注24 h,NAC组LDH和TnT的活性亦均降低(P<0.05),CK-MB的活性未见明显变化,SFN组血清中CK-MB和TnT的活性亦均降低(P<0.05);NAC组和SFN组心肌组织学及超微结构的损伤程度均较对照组明显减轻;与对照组相比,NAC组心肌组织SOD活性及SOD/LPO比值明显升高(P<0.05),LPO含量未见明显变化(P>0.05);SFN组供心心肌组织LPO含量显著降低(P<0.05),SOD活性未见明显变化,SOD/LPO明显提高(P<0.01)。结论:SFN能保护移植心脏,其机制可能与其诱导Ⅱ期酶产生,提高心肌细胞对氧化应激的防御能力,减少自由基对心肌的氧化损伤有关。
Objective To investigate the effect of sulforaphane （SFN） on myocardial ischemia reperfusion injury in rats heart transplantation. Methods 60 healthy male Lewis rats were randomly divided into control, NAC group and SFN group （each n = 20）. Recipient rats were injected the equal amount saline via tail vein 24 hours before heart transplantation in control group. Recipient rats were injected NAC 300 mg/kg via tail vein 24 hours before heart transplantation in NAC group. Recipient rats were injected SFN 2.5 mg/kg via vena cava 24 hours before heart transplantation in SFN group. And donnor rats＇ hearts after taken out were stored in 4 ~C HTK solution for 18 hours in all groups. Heart transplantation was performed according to Ono＇s method. The function recovery of heart graft was evaluated by semi-quantitative method after heart transplantation. Blood was drawn at 6, 24 hours post-reperfusion for analysis of LDH, CK-MB, TnT. Tissue samples were taken 24 h after reperfusion for histology and uhrastructural changes. Graft SOD, LPO activity was detected 24 h after reperfusion. Results Graft function in SFN group and NAC group were significantly improved compared with control group （P 〈 0.05）. Compared with control group, the levels of LDH, CK-MB, TnT were significantly reduced in NAC and SFN groups at 6 h and 24 h after reperfusion （P 〈 0.05）. Histology （H.E staining and electron microscopy） also proved that SFN and NAC pretreatment groups were better than control. The activity of SOD and SOD/LPO were significant increased in NAC group （P 〈 0.05）, but the levels of LPO were not significant difference compared with control group （P 〉 0.05）. The level of LPO was significantly decreased （P 〈 0.05）, SOD/LPO was significantly increased （P 〈 0.01 ）, but the activity of SOD was not significant difference in SFN group compared with control group. Conclusions SFN protects the heart graft. The mechanism of protection may be attributable to induce the expression of phase 11 enzymes, improve the defense capability of the myocardial cells against oxidative stress, reduce the free radicals on the myocardial oxidative damage.
出处
《实用医学杂志》
CAS
北大核心
2013年第23期3850-3852,共3页
The Journal of Practical Medicine
基金
留学回国人员科研启动基金项目(编号:教外司留2010-1561-25)
关键词
心脏移植
莱菔硫烷
冷缺血再灌注损伤
氧化应激
Heart transplation
Sulforaphane
Cold ischemia reperfusion injury
Oxidative stress
