目的 探讨甘利欣注射液对博莱霉素所致肺纤维化大鼠血清α-平滑肌肌动蛋白（α-SMA）、Ⅱ型肺泡表面抗原-6（KL-6）和核因子κB（NF-κB）的影响。方法 取健康Wistar大鼠50只，随机分为5组，即正常组、模型组和甘利欣注射液低、中、高剂量组（25，50，100 mg·kg-1）。除正常组外，其余各组经气道注入博莱霉素复制肺纤维化动物模型，正常组用等容量生理盐水经大鼠气道注入。模型复制后第28天开始，腹腔注射甘利欣注射液，连续14 d。第15天处死大鼠，取左肺下叶的组织，用实时荧光PCR和免疫组化检测α-SMA mRNA、NF-κB mRNA表达；大鼠右肺下叶HE染色观察病理学切片。取大鼠血清用ELISA双抗体夹心法测定α-SMA、KL-6和NF-κB的含量。结果 甘利欣各组大鼠肺纤维化程度均较轻微，模型组大鼠肺组织成纤维细胞反应增强。正常组和甘利欣各组大鼠肺组织α-SMA mRNA、NF-κB mRNA表达较低，α-SMA和NF-κB染色及定量表达减弱，与模型组比较，差异有统计学意义（P＜0.05）。正常组和甘利欣各组大鼠血清α-SMA、KL-6和NF-κB含量与模型组比较，差异有统计学意义（P＜0.05）。结论 甘利欣注射液能够减少肺组织α-SMA、NF-κB的表达，降低α-SMA、KL-6和NF-κB含量，进而减轻肺组织纤维化程度。

Objective To investigate the effect of Diammonium Glycyrrhizinate Injection（DGI）on alpha smooth muscle actin（α-SMA），type Ⅱpulmonary alveolus surface antigen 6（KL-6） and nuclear factor kappa B（NF-κB） in rat model of pulmonary fibrosis induced by Bleomycin. Methods Fifty rats were randomly divided into 5 groups，normal group，pulmonary fibrosis group（model group），and low-，middle- and high-dose DGI groups（in the dosage of 25，50，100 mg·kg-1）. Rats except for the normal group were given infusion of Bleomycin through the airway to induce pulmonary fibrosis，and the normal group was given the same volume of normal saline through the airway. On the modeling day 28，DGI was given to the model rats by intraperitoneal injection for 14 continuous days. On the medication day 15，rats were executed，left inferior lung tissues were taken out for the detection ofα-SMA mRNA and NF-κB mRNA expression by real time fluorescence PCR，and the right lung was made into slice for the pathological observation. Serum α-SMA，KL-6 and NF-κB contents were measured by ELISA. Results The pulmonary alveolitis and fibrosis of DGI groups were significantly milder than pulmonary fibrosis group. Pulmonary α-SMAr mRNA and NF-κB mRNA and protein expression levels were lower in the normal group and DGI groups than the model group（P＜0.05）. Serum α-SMA，KL-6 and NF-κB contents in the normal group and DGI groups differed from those in the model group（P＜0.05）. Conclusion DGI has certain effect on relieving rat pulmonary fibrosis through reducing pulmonary α-SMA abd KL-6 expression，and by decreasing serumα-SMA，KL-6 and NF-κB contents in rats

R285.5

海南省卫生厅科研课题（2011-SWK-06-132/琼卫2011-61）。