摘要
作者在大鼠失血性休克（４ｋＰａ，１８０分钟）模型上，观察了重组杀菌／通透性增加蛋白（ＢＰＩ）对肺组织肿瘤坏死因子（ＴＮＦ）、白介素－６（ＩＬ－６）ｍＲＮＡ表达及急性肺损伤的影响，并对肠源性内毒素血症与炎症细胞因子诱发的关系进行了探讨。结果显示：失血性休克可导致血浆内毒素含量显著升高，肺组织ＴＮＦ、ＩＬ－６ｍＲＮＡ表达分别在复苏后２、８小时明显增多（Ｐ＜０．０５～０．０１）；给予ＢＰＩ治疗则完全中和休克所致内毒素血症，并不同程度地抑制肺组织ＴＮＦ、ＩＬ－６ｍＲＮＡ的表达（Ｐ＜０．０５～０．０１）；肺毛细血管通透性与髓过氧化物酶活性均明显降低。作者认为，ＢＰＩ可有效防止失血性休克诱发的急性肺损伤，其作用机制可能与抑制肠源性内毒素血症所介导的局部组织炎症细胞因子基因表达有关。
To determine the possible mechanisms underlying beneficial effect of recombinant bactericidal/permeability increasing protein (rBPI) on acute lung injury response to blood loss, we used reverse transcription polymerase chain reaction to measure pulmonary tumor necrosis factor (TNF), interleukin 6 (IL 6) mRNA expression in a rat model of prolonged hemorrhagic shock (4 00kPa, 180 min) followed by adequate resuscitation. The results showed that systemic plasma endotoxin concentrations elevated rapidly after a 180 min hemorrhagic insult ( P <0 05),and TNF,IL 6 mRNA expression in the lung were significantly increased at 2,8 hours after resuscitation respectively. However,treatment with rBPI resulted in almost neutralization of plasma endotoxin values,remarkable reduction of TNF,IL 6 mRNA levels following hemorrhage/resuscitation. Also,it was found that rBPI administration markedly blunted the increase in pulmonary Evans blue dye extravasation,concomitant with a significant decrease in lung myeloperoxidase activity compared with the control group ( P <0 05～0 01). These data suggest that local proinflammatory cytokine mRNA expression associated with gut origin endotoxemia may be an important mechanism contributing to the development of hemorrhage induced lung injury. Treatment with rBPI is effective in inhibiting marked TNF,IL 6 mRNA expression and ameliorating acute lung injury secondary to severe hemorrhagic shock.
出处
《中华外科杂志》
CAS
CSCD
北大核心
1997年第7期389-391,共3页
Chinese Journal of Surgery
基金
全军医药卫生科研基金
奥地利科学发展促进会基金
关键词
出血性休克
呼吸窘迫综合征
BPI
MRNA
Shock,hemorrhagic Respiratory distress syndrome Recombinant proteins Cytokines Gene expression
