实用医学杂志 ›› 2022, Vol. 38 ›› Issue (5): 577-582.doi: 10.3969/j.issn.1006⁃5725.2022.05.011

• 基础研究 • 上一篇    下一篇

乳果糖对失血性休克大鼠急性肺损伤的作用及机制

郑强1 唐勇1 周程继1 谷子1 刘世平2    

  1. 1 成都市第二人民医院急诊科(成都617000);2 川北医学院附属医院急诊科(四川南充637000)

  • 出版日期:2022-03-10 发布日期:2022-03-10
  • 通讯作者: 刘世平 E⁃mail:liusp456@163.com
  • 基金资助:
    四川省卫生和计划生育委员会重点研究项目(编号:17ZD016)

The effect and mechanism of lactulose on acute lung injury in hemorrhagic shock rats

ZHENG Qiang*, TANG Yong,ZHOU Chengji,GU Zi,LIU Shiping.   

  1. Department of Emergency,Chengdu Second People′s Hospital Chengdu 617000,China

  • Online:2022-03-10 Published:2022-03-10
  • Contact: LIU Shiping E⁃mail:liusp456@163.com

摘要:

目的 探讨乳果糖对失血性休克大鼠急性肺损伤的作用及机制。方法 失血性休克模型制 备前60 min,先分为乳果糖预灌胃组即实验组2(10只)。将实验组2及未进行乳果糖预灌胃处理的 SD 大鼠 同时麻醉,左右股动静脉置管成功后再将未进行乳果糖预灌胃处理的 SD 大鼠分为三组:假手术组即空白 组(10 只)、生理盐水复苏组即对照组(10 只)、乳果糖治疗组即实验组 1(10 只)。四组实验动物置管成功 后制备失血性休克模型,持续监测生命体征。在 0、30 270 min 分别测定血气和乳酸值。Western法检测 270 min肺组织HMGB1;Elisa法检测270 min血IL⁃6、IL⁃1β;用比色法检测270 min肺组织 SOD MDA;TBA 法检测 270 min 肺组织 MPO;光镜下分析 270 min 肺组织病理切片。结果 270 min 时,对照组 Po2值明 显低于空白组、实验组 1 及实验组 2(P < 0.05)。空白组 IL⁃6、IL⁃1β、SOD、MDA、MPO 分别与对照组、实验 1及实验组2比较差异有统计学意义(P < 0.05);对照组与实验组2、实验组1与实验组2比较差异均有统 计学意义(P < 0.05)。对照组 HMGB1 分别与空白组、实验组 1 及实验组 2 比较差异有统计学意义(P < 0.05)。在肺病理学切片结果显示实验组 1 较实验组 2 肺泡内皮及肺泡组织明显破坏,炎性细胞浸润明 显。对照组较实验组 1 及实验组 2 肺泡内皮及肺泡组织破坏及炎性细胞浸润更加明显。结论 在失血性休克动物模型中,乳果糖可促进 SOD 的生成并抑制 HMGB1 的生成,进而抑制 IL⁃6、IL⁃1β、MDA、MPO 等炎 性介质的释放,保护肺组织。

关键词:

乳果糖, 失血性休克, 肺损伤, SD 大鼠

Abstract:

Objective The aim of this study was to evaluate the effect and mechanism of lactulose on acute lung injury in rats with hemorrhagic shock. Methods SD rats without lactulose pretreatment were divided into three groups:sham operation group(10 rats),normal saline resuscitation group(10 rats),and lactulose treatment group(1 rats)(10 animals)ahead of 60 min before preparation of hemorrhagic shock. After the successful catheterization of the four groups of experimental animals,the hemorrhagic shock model was prepared and the vital signs were continuously monitored. The blood gas and lactic acid values were measured at 0 min,30 min and 270 min. The HMGB1 in lung tissue was detected by western method and the IL⁃6 as well as IL⁃1 in blood were detect⁃ ed by ELISA method β. SOD and MDA in lung tissue were detected by colorimetry at 270 min. The expression of MPO in lung tissue was detected by TBA at 270 min. The pathological sections of lung tissue were analyzed under light microscope. Results At 270min,the pO2 value of the control group was significantly lower than that of the blank group,experimental group 1 and experimental group 2(P < 0.05). IL⁃6,IL⁃1 β,SOD,MDA and MPO in blank group were statistically significant different with control group,experimental group 1 and experimental group 2 respectively(P < 0.05). The comparison between control group and experimental group 2 was also statistically significant different(P < 0.05). Compared with experimental group 2,experimental group was also statistically significant different(P < 0.05). HMGB1 in control group was statistically significant different with blank group experimental group 1 and experimental group 2 respectively(P < 0.05). The results of lung pathological sections showed that the alveolar endothelium and alveolar tissue in experimental group 1 were significantly damaged and inflammatory cell infiltration was significant obviously when comparing with experimental group 2. The destruction of alveolar endothelium and alveolar tissue and inflammatory cell infiltration in the control group were more obvious than those in experimental group 1 and experimental group 2. Conclusion Lactulose could promote the production of SOD and inhibit the production of HMGB1,and thus inhibit the release of IL⁃6,IL⁃1 β,MDA,MPO and other inflammatory mediators for protecting the lung tissue.

Key words:

lactulose, hemorrhagic shock, injury of lungs, SD rats