摘要
目的:探讨虎杖甙(PD)抗肺缺血/再灌注损伤作用及其机制。方法:采用在体兔单肺原位缺血/再灌注损伤模型。健康日本大耳白兔40只随机均分成4组(n=10):假手术对照组(C组);肺缺血/再灌注组(I/R组);肺缺血/再灌注+虎杖甙组(PD组),缺血前20 min和再灌注即刻按2.5 mg/kg静脉注射0.2%PD溶液;肺缺血/再灌注+PD+多粘菌素B组(PMB组),给PD同时按24 mg/kg静注PMB。各组分别在缺血前20 min,缺血1 h即刻,再灌注1 h、2 h、3 h各时点颈动脉抽血检测丙二醛(MDA)含量,超氧化物歧化酶(SOD)活性。实验结束时,取肺组织测湿干重比(W/D),计算肺泡损伤率(IAR),电镜观察细胞超微结构改变。结果:①I/R组和PMB组血清SOD活性随着缺血和再灌注时间的延长而逐渐下降,且两组间无差异;PD组则显著改善(均P<0.01)。②I/R组、PD组、PMB组血清MDA浓度均随着缺血和再灌注时间的延长而逐渐上升,但PD组上升明显缓慢(均P<0.01)。③I/R组、PD组和PMB组的W/D与IAR均高于C组(P<0.05或P<0.01),但PD组显著低于I/R组和PMB组(均P<0.01)。④I/R组及PMB组肺组织的超微结构损伤严重,PD组损伤程度明显较轻。结论:PD对肺缺血/再灌注损伤具有拮抗作用,其机制除抗氧化损伤外可能还有PKC参与。
Aim： To observe protective effects of polydatin （PD） during lung ischemia/reperfusion injury （LI/RI） and investigate its potential mechanism. Methods： Rabbit lung model of ischemia/reperfusion injury was constituted in vivo. The 40 rabbits were randomly divided into four groups （n= 10） ： control group（C group）, ischemia/reperfusion group （I/R）, PD＋ I/R group （PD） and PD＋ polymyxin B （PMB） ＋ I/R group （PMB）. The blood specimen gathered at different time points were tested for the content of mdondialdehyde （MDA） and the enzyme activity of superoxide dismutase （SOD）. The lung tissue ,sampled at the end of the experiment were assayed for wet/dry weight ratio （W/D）, injured alveoli rate （IAR） and observing ultrastructure changes under electron microscope. Results：（1）The activity of SOD showed a similar time-dependent decline in I/R group and PMB group during I/R, while in PD group this tendency was milder （P〈0.01 vs I/R group）. （2）In contrast to the results above, the level of MDA markedly increased in I/R and PMB group, but was slowed down in PD group （P〈0.01 vs I/R group）. （3）The value of W/D and IAR was much higher in I/R and PMB group （ P 〈 0.05 or P 〈 0.01 vs C group）. In PD group, it was decreased （ P 〈 0.01 vs I/R group or PMB group）. （4） Electron microscope showed obvious ultrastructure injury brought by LI/RI in I/R group and PMB group, which was greatly attenuated in PD group. Conclusion： PD can protect lung from LI/RI, and PKC may participate in its mechanisms.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2008年第1期62-65,共4页
Chinese Journal of Applied Physiology
基金
浙江省卫生厅科研基金资助项目(SWS00021)
关键词
虎杖甙
肺
缺血/再灌注损伤
polydatin
lung
ischemia/reperfusion injury
