摘要
目的:探讨灵芝多糖(GLP)对失血性休克再灌注复苏时肠粘膜损伤的保护作用及机制。方法:复制家兔失血性休克再灌注复苏模型,随机分成假手术组(S组)、生理盐水再灌注复苏组(NS组)和质量分数为1%的GLP再灌注复苏组(LS组),于放血前、休克40min、再灌注复苏40min和90min时观察细菌的移位情况;复苏90 min时,检测肠粘膜SOD活性、MDA和TNFα含量的变化;同时取回肠末端观察肠粘膜的损伤情况和用TUNEL法检测肠粘膜细胞凋亡情况。结果:1随着再灌注复苏时间的延续,NS组血液细菌阳性率增加,细菌移位增加,明显高于LS组和S组(P<0.05);2NS组和LS组肠粘膜SOD活性明显低于S组,而LS组又明显高于NS组(P<0.05);NS组和LS组肠粘膜MDA和TNFα含量明显高于S组,而LS组又明显低于NS组(P<0.05);3NS组肠粘膜损伤明显重于S组和LS组,且肠粘膜凋亡细胞百分数也明显高于S组和LS组(P<0.05)。结论:失血性休克再灌注复苏过程中肠粘膜的损伤与局部脂质过氧化反应增强、TNFα介导的炎症反应及肠粘膜细胞的凋亡增多等有关,而GLP对此损伤有保护作用。
Objective： To study the protective effects of GLP on intestinal mucosa injury in hemorrhagic shock reperfusion and its mechanism. Methods：With the model of HS-R in rabbits, the animals were divided into three groups： sham operation group （S group）, reperfusion with N-S group （NS group）, reperfusion with 1% GLP group （LS group）. The incidence rates of bacterial translocation were observed at the time of pre-shock, shock 40 min, post-reperfusion 40 min and 90 min respectively. The changes of SOD, MDA and TNFα in intestinal mucosa were examined at the time of post reperfusion 90 min, meanwhile the degree of intestinal injury and the apoptosis of intestinal mucosa were all examined. Results： （1） With the extension of reperfusion time the positive rate of blood bacteria increased gradually in NS group, which was significantly higher than that in S group and LS group （P〈0.05）. （2） The activity of SOD in intestinal mucosa of NS group and LS group were significantly lower than that in S group （P〈0. 05） , but its activity in LS group was significantly higher than those in NS group （P〈0.05）. The contents of MDA and TNFα in intestinal mucosa of NS group and LS group were significantly higher than those in S group （P〈0.05） , but their contents in LS group was significantly lower than those in NS group （P〈0.05）. （3）The degree of intestinal injury in NS group was more severe than that in S group and LS group （P〈0. 05）. The percentage of the apoptotic cells in intestinal mucosa of NS group were significantly higher than that of LS group and S group. Conclusion： The intestinal mucosa injury in HS-R is related with lipid peroxidation, inflammatory response induced by TNFα and the increasing of the apoptotic cells in intestinal mueosa, meanwhile GLP has protective effect on intestinal mucosainjury in HS R.
出处
《陕西医学杂志》
CAS
2010年第2期134-136,共3页
Shaanxi Medical Journal
基金
河南省教育厅自然科学研究项目(2006310021)
