IL-38在大鼠肺间质纤维化模型中的作用研究

Role of IL-38 in rat interstitial pulmonary fibrosis model

目的采用气管内注射博来霉素(BLM)的方法构建大鼠肺间质纤维化模型,探讨IL-38在肺间质纤维化中的作用及意义。方法运用随机数字表法将60只健康Wistar大鼠分为盐水对照组(N组,20只)、单纯博来霉素组(B组,20只)、地塞米松干预组(D组,20只)。D组从第二天开始给予地塞米松腹腔注射,1次/日,连续至28天。光镜下观察肺组织的病理形态,测定大鼠血清、肺组织匀浆中IL-38表达量,采用RT-PCR法测定大鼠肺组织MIP-2的表达量。结果①D组肺损伤及肺纤维化程度较同期B组均明显减轻。②与同期N组对比,B、D组大鼠血清及肺组织匀浆中IL-38的表达量均减少(P <0. 05);与同期B组对比,D组大鼠血清及肺组织匀浆中IL-38的表达量均增加(P <0. 05)。③与同期N组对比,B、D组大鼠肺组织内MIP-2的表达量均增加(P <0. 05);与同期B组对比,D组大鼠肺组织内MIP-2的表达量减少。结论 IL-38表达不足在博来霉素致大鼠肺间质纤维化形成中有重要作用,通过刺激IL-38的表达,增加可能会改善大鼠肺间质纤维化程度。

Objective To construct a rat model of interstitial pulmonary fibrosis by intratracheal injection of bleomycin(BLM),and to explore the role and significance of IL-38 in pulmonary fibrosis.Methods 60 healthy Wistar rats were divided into the saline control group(the group N,20),the simple bleomycin group(the group B,20),and the dexamethasone intervention group(the group D,20 rats).The group D was daily given intraperitoneal injection of dexamethasone from the second day for 28 days.The pathological morphology of lung tissue was observed under light microscope,and the expression of IL-38 in serum and lung homogenate of rats was measured.The expression of MIP-2 in lung tissue of rats was measured by RT-PCR method.Results Lung injury and pulmonary fibrosis in the group D were significantly lower than those in the group B at the same time.Compared with the same period at the N group,the expression of IL-38 in serum and lung homogenate of the groups B and D decreased(P<0.05),and the expression of IL-38 in serum and lung homogenate of the group D increased(P<0.05).(3)Compared with the N group,the expression of MIP-2 in the lung tissue of the groups B and D increased(P<0.05),and the expression of MIP-2 in the lung tissue of the group D decreased compared with that of group B at the same time.Conclusion The insufficient expression of IL-38 plays an important role in the formation of pulmonary fibrosis induced by bleomycin in rats.The increase of IL-38 expression may improve the degree of pulmonary fibrosis in rats.