Department of Pneumology, Gaomi Hospital of Traditional Chinese Medicine, Gaomi 261500, China.
Department of Obstetrics and Gynecology, People's Hospital of Gaomi, Gaomi 261500, China.
Cell Mol Biol (Noisy-le-grand). 2020 Jun 5;66(3):79-84.
This study aimed to explore the effects of miR-27a-3p-mediated Smurf2 on bleomycin A5-induced pulmonary fibrosis in rats. Sixty clean-grade SD rats were made into models of pulmonary fibrosis induced by bleomycin A5. They were randomly divided into the control group (fed as usual), the bleomycin A5 group, and the miR-27a-3p group according to the modeling. Pathological sections and morphological observations were performed on the lung tissues of all rats, and the expression of miR-27a-3p, Smurf2 mRNA, Smurf2 protein, collagen type I (Col I), collagen type III (Col III), and related inflammatory factors in lung tissues were measured. Dual fluorescein detection was performed for miR-27a-3p and Smurf2 in lung tissues. The lung tissue of rats in the bleomycin A5 group showed obvious pathological changes. The degree of pulmonary fibrosis in the miR-27a-3p group was significantly lower than that in the bleomycin A5 group. The expression levels of Smurf2 mRNA, Smurf2 protein, Col I, Col III, and related inflammatory factors in the lung tissue of rats in the control group were notably lower than rats in the bleomycin A5 group and the miR-27a-3p group (levels of those factors in the miR-27a-3p group were lower than the bleomycin A5 group). The expression level of miR-27a-3p in the lung tissue of rats in the control group was significantly higher than that in the bleomycin A5 group and the miR-27a-3p group (miR-27a-3p level in the miR-27a-3p group was significantly higher than in the bleomycin A5 group). Results of dual fluorescein detection demonstrated that Smurf2 was a direct target gene of miR-27a-3p, and the expression of miR-27a-3p negatively associated with Smurf2. Up-regulation of miR-27a-3p expression can effectively improve the disease degree and inflammatory response in rats with pulmonary fibrosis. Its mechanism may be achieved by regulating Smurf2.
本研究旨在探讨 miR-27a-3p 介导的 Smurf2 对博来霉素 A5 诱导的大鼠肺纤维化的影响。
将 60 只清洁级 SD 大鼠制成博来霉素 A5 诱导的肺纤维化模型。根据建模情况，将它们随机分为对照组（常规喂养）、博来霉素 A5 组和 miR-27a-3p 组。对所有大鼠的肺组织进行病理切片和形态学观察，并测量肺组织中 miR-27a-3p、Smurf2mRNA、Smurf2 蛋白、胶原 I（Col I）、胶原 III（Col III）和相关炎症因子的表达。对肺组织中的 miR-27a-3p 和 Smurf2 进行双荧光素检测。
博来霉素 A5 组大鼠的肺组织出现明显的病理变化，miR-27a-3p 组的肺纤维化程度明显低于博来霉素 A5 组。对照组大鼠肺组织中 Smurf2mRNA、Smurf2 蛋白、Col I、Col III 和相关炎症因子的表达水平明显低于博来霉素 A5 组和 miR-27a-3p 组（miR-27a-3p 组的这些因子水平低于博来霉素 A5 组）。对照组大鼠肺组织中 miR-27a-3p 的表达水平明显高于博来霉素 A5 组和 miR-27a-3p 组（miR-27a-3p 组的 miR-27a-3p 水平明显高于博来霉素 A5 组）。双荧光素检测结果表明，Smurf2 是 miR-27a-3p 的直接靶基因，miR-27a-3p 的表达与 Smurf2 呈负相关。上调 miR-27a-3p 的表达可以有效改善肺纤维化大鼠的疾病程度和炎症反应。其机制可能是通过调节 Smurf2 实现的。
