生地提取物对肺间质纤维化大鼠肺系数及MCP-1 mRNA表达的影响

Influences of Shengdihuang(Rehmanniae recens Radix) Extract on Pulmonary Index and Monocyte Chemoattractant Protein-1 mRNA Expression of Pulmonary Interstitial Fibrosis Rats

目的检测生地提取物对肺间质纤维化模型大鼠肺系数及MCP-1 mRNA表达的影响并初步研究其作用产生的内在机理。方法博莱霉素气管内注入法复制大鼠肺间质纤维化模型。随机分为正常组、模型组、生地提取物组和甲强龙组,各组分别在造模后第3、7、28天处死总数的1/3只,取全肺称重,计算肺系数,并用逆转录多聚酶链反应(RT-PCR)方法,检测MCP-1 mRNA的表达。结果第28天生地提取物组和甲强龙组肺系数较模型组有减小趋势。MCP-1 mR-NA的表达在肺间质纤维化过程中增加,第7天时达到高峰,模型组MCP-1 mRNA的表达高于正常组(P <0. 05),第28天时已有回落。生地提取物组和甲强龙组第7天和第28天MCP-1 mRNA均有低于模型组的趋势。结论生地提取物可改善肺间质纤维化模型大鼠肺系数;生地提取物抑制肺间质纤维化过程中MCP-1mRNA的表达,从而可能延缓大鼠肺纤维化的形成。

Objective To investigate influences of Shengdihuang( Rehmanniae recens Radix) extract on pulmonary index and expression of monocyte chemoattractant protein-1( MCP-1) mRNA,for the preliminary study of the internal mechanism. Methods The model of pulmonary interstitial fibrosis in rats was reproduced by bleomycin endotracheal injection. They were randomly divided into the normal group,the model group,the Shengdihuang extract group and the methylprednisolone group. 8 rats in each group were sacrificed on the 3 rd,7 th and 28 th day after the intratracheal instillation. The weight and pulmonary index were counted. The mRNA of( MCP-1) was determined by reverse transcription-polymerase chain reaction( RT-PCR). Results On the 28 th day,the pulmonary index had a downward trend on the Shengdihuang extract group and the methylprednisolone group,compared to the model group. The expression of MCP-1 mRNA increased during pulmonary interstitial fibrosis,and peaked on the 7 th day. The expression of MCP-1 mRNA in the model group was higher than that in the normal group( P < 0. 05),and it fell back on the 28 th day. The trend of MCP-1 mRNA both in the Shengdihuang extract group and the methylprednisolone group was lower than the model group on the 7 th and 28 th day. Conclusion Shengdihuang extract can improve pulmonary index of the pulmonary fibrosis rats,and inhibit the expression of MCP-1 mRNA during pulmonary interstitial fibrosis,which may delay the formation of pulmonary fibrosis in rats.