赤芍对大鼠内毒素性急性肺损伤时肺iNOS和eNOS表达的影响

目的 :观察赤芍对内毒素性急性肺损伤 (ALI)时肺iNOS和eNOS表达的影响 ,并探讨其保护作用机制。方法 :采用大鼠内毒素ALI模型。 4 0只Wistar大鼠随机分为生理盐水对照组 (NS)、内毒素组 (LPS)、赤芍治疗组、赤芍预防组和iNOS阻断剂氨基胍 (AG)组。应用免疫组织化学方法和图像分析系统检测肺组织中iNOS和eNOS的表达 ,检测血清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NS组比较 ,LPS组iNOS表达显著增强而eNOS表达明显降低 (均P <0 .0 1) ;赤芍治疗组和赤芍预防组iNOS表达较LPS组明显降低而eNOS表达明显升高 (均P <0 .0 5 ) ;与LPS组比较 ,AG组仅iNOS表达明显降低。LPS组肺组织MDA和血清NO较NS组明显增加 (P <0 .0 1) ;与LPS组比较 ,赤芍治疗组和赤芍预防组MDA含量和血清NO显著降低 (P <0 .0 5或P <0 .0 1)。病理学检查显示赤芍治疗组和赤芍预防组肺组织损伤程度较LPS组明显减轻。结论 :肺组织iNOS表达增强和eNOS表达降低是内毒素性ALI的重要机制 ,赤芍对内毒素性ALI的防治作用可能与抑制肺组织iNOS异常高表达和增加eNOS表达有关。

Effect of Radix Paeoniae Rubra on Expression of iNOS and eNOS in Lipopolysaccharide-induced Acute Lung Injury

Objective: To investigate the effect of Radix Paeoniae Rubra(RPR) on expression of iNOS and eNOS in lipopolysaccharide-induced acute lung injury(ALI) and to explore it's protective mechanism. Methods: Forty Wistar rats were divided randomly into 4 group: normal saline control(NS) group, lipopolysaccharide(LPS)group, RPR for treatment group, RPR for prevention group and AG group. Models of endotoxin induced ALI were used to observe MDA content in lung and the activities of serum NO. Expression of iNOS and eNOS in rat lung tissue was detected by immunohistochemical methods and morphometry computer image analysis. The histological changes of lung were observed under optical microscope. Results: Compared with that in NS group, expression of iNOS was markedly increased while expression of eNOS was significantly decreased in LPS group (P<0 01). But in RPR for treatment group and RPR for prevention group, expression of iNOS was significantly lower than that in LPS group and expression of eNOS was obviously higher than that in LPS group(P<0 05).The content of MDA and the activities of serum NO in LPS group were significantly higher than those in NS group (P<0.01). Compared with those in LPS group, the content of MDA and the activities of serum NO were significantly lower in RPR for treatment group and RPR for prevention group (P<0.05 or P< 0.01 ). Under microscope, the pathologic changes induced by LPS were significantly attenuated by RPR and AG. Conclusion: The high-expression of iNOS and the low-expression of eNOS play important roles in lipopolysaccharide-induced acute lung injury. Protective effect of RPR on lipopolysaccharide-induced acute lung injury is related to the inhibition of iNOS expression and the inducement of eNOS expression.