摘要
目的观察赤芍对内毒素(LPS)性急性肺损伤(ALI)时肺诱导型血红素氧化酶(HO-1)和诱导型一氧化氮合酶(iNOS)表达的影响,探讨其保护作用及分子机制。方法40只Wistar大鼠随机分为对照组、内毒素组(LPS组)、赤芍治疗组、赤芍预防组和血晶素组,每组8只。采用大鼠内毒素ALI模型,于LPS滴注后6h取动脉血行血气分析,测定肺组织中HO-1和iNOS的表达,肺泡灌洗液中性粒细胞比、蛋白含量,血清一氧化氮(NO)及肺组织丙二醛(MDA)含量,同时观察肺组织病理形态学改变。结果与对照组比较,LPS组HO-1和iNOS表达显著增强(P<0.01),肺泡灌洗液中性粒细胞比、蛋白含量、肺组织MDA和血清NO显著增加,而PaO2和HCO3ˉ明显降低(P<0.01);与LPS组比较,赤芍治疗组、赤芍预防组和血晶素组HO-1表达明显升高,而iNOS表达明显降低(P<0.05),病理学检查显示肺组织损伤程度较LPS组明显减轻。结论肺组织HO-1表达增强是内毒素性ALI的重要应激保护机制,赤芍对内毒素性ALI的防治作用可能与诱导HO-1的表达和抑制肺组织iNOS异常高表达有关。
Objective To investigate the effect of radix paeoniae rubra （RPR） on expression of heme oxygenase （ HO-1 ） and inducible nitric oxide synthase （iNOS） in lipopolysaccharide （ LPS）-induced acute lung injury （ALI） and explore its protective mechanism. Methods Forty Wistar rats were randomly and equally divided into five groups, ie, control group, LPS group, RPR treatment group, RPR prevention group and Hemin group. Arterial blood was drawn for blood gas analysis. Models of endotoxin- induced ALI were used to observe the protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid （ BALF）, the malondialdehyde （MDA） content in lung and the activities of serum NO. Expression of HO-1 and iNOS in rat lung tissue was detected by immunohistochemistry and morphometry computer image analysis. The histological change of lung were observed under light microscope. Results Compared with control group, expression of HO-1 and iNOS was markedly increased （ P 〈 0.01 ） , the protein content, the ratio of neutrophiles in BALF, MDA content and the activities of serum NO were significantly higher in LPS group （P 〈 0.01 ）. Compared with LPS group, RPR treatment group, RPR prevention group and Heroin group, expression of HO-1 was obviously higher while expression of iNOS was significantly lower （P 〈 0.05 ）. Under light microscope, the pathologic changes induced by LPS were significantly attenuated by RPR and Hemin. Conclusion High expression of HO-1 is important stress protective mechanism. While protective effect of RPR on LPS-induced ALl is related to the inhibition of iNOS expression and the inducement of HO-1 expression.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2005年第9期675-678,共4页
Chinese Journal of Trauma
基金
湖北省教育厅立项课题资助项目(2003X125)
