复方甘草甜素对肺纤维化大鼠INF-γ／IL-4细胞因子的影响

目的：观察复方甘草甜素对肺纤维化大鼠血清IFN-γ、IL-4表达水平的影响，探讨复方甘草甜素对肺纤维化的治疗作用及可能的作用机制。方法：72只SD健康大鼠，随机分为4组（每组各18只）：空白对照组、模型对照组、地塞米松阳性对照组、甘草甜素治疗组。模型对照组、地塞米松阳性对照组和甘草甜素治疗组气管内注射博莱霉素诱导肺纤维化模型，空白对照组在相同条件下给予生理盐水。甘草甜素治疗组和地塞米松阳性对照组每天分别给予复方甘草甜素2mL／100g腹腔内注射，地塞米松注射液0．03mg／100g腹腔内注射，其余两组每天生理盐水2mL／100g腹腔内注射。各组分别于造模后第7、14、28天各处死6只大鼠，取大鼠血清和肺组织。肺组织病理切片HE染色和MASSON染色观察病理变化和肺纤维化分级情况，ELISA法测定血清中INF-γ、IL-4含量的变化。结果：与模型对照组比较，甘草甜素治疗组各个时期的血清IFN-1表达明显增高（P〈0．05）；地塞米松阳性对照组大鼠血清IL-4在各个时期的表达降低明显（P〈0．05），尤其在第7天下降明显，比甘草甜素治疗组更低（P〈0．05）。结论：复方甘草甜素对肺纤维化的形成有较好的治疗作用，其机制可能是早期通过促进血清中IFN-叫的分泌，抑制IL-4的分泌，从而调节了Th1／Th2细胞因子失衡，减轻肺泡炎来实现的，后期通过上调INF-γ水平对肺纤维化的抑制作用。

Experimental Study on Effect of Stronger NEO-Minophagen C Cytokines on INF-γ and IL-4 Serum Level in Rats with Pulmonary Fibrosis

Objective To observe the influence of Stronger NEO-Minophagen C （SNMC） on the level of serum INF- γ and IL-4 in rats with pulmonary fibrosis induced by bleomycin, and investigate the treatment and its mechanism of SNMC in rats with pulmonary fibrosis. Methods 72 healthy SD rats were randomly divided into 4 groups （n=lS, each）： control group （group A）, model group （group B）, DXM group （group C）, SNMCgroup （group D）. The rats of group B, C, D were injected bleomycin in trachea to induce pulmonary fibrosis, the rats of group A was injected NS, and respective medicine was given to each group. Every group was subdivided into three groups （n =6） which was killed in the 7th, 14th and 28th day respectively. Then, the serum and lung tissues were sampled. The pathological changes of lung tissues were observed by HE staining and MASSON staining to rating pulmonary fibrosis. TNF-γ and IL-4 serum levels were measured by ELISA. Results Comparing with model group, INF- γ/ serum level of SNMC group was significantly increased （P 〈 0.05）; IL-4 serum level of DXM group was significantly reduced （P 〈 0.05）, especially in the 7th day, was lower than SNMC group （P 〈 0.05）. Conclusion SNMC showed a significant effect on pulmonary fibrosis, and the mechanism may be promoting the secretion of INF-γ and inhibiting the secretion of IL-4 in serum, accordinglyadjusting the imbalance of cytokines Thl/Th2, reducing the alveolitis in early stage; and increacing the level of INF- γ/ to inhibit pulmonary fibrosis in later stage.