miR-26b和miR-27b表达的研究以及槲皮素对实验性肺纤维化纤维化的影响。

IF 2.9 4区 生物学 Q3 CELL BIOLOGY Journal of Molecular Histology Pub Date : 2023-10-19 DOI:10.1007/s10735-023-10168-z
Çağrı Toker, Yurdun Kuyucu, Dilek Şaker, Samet Kara, Bilge Güzelel, Ufuk Özgü Mete
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引用次数: 0

摘要

本研究旨在研究槲皮素对博莱霉素诱导的肺纤维化和纤维化相关分子miR-26b和miR-27b的影响。对照组于第0天给予10%生理盐水,从第8天开始给予生理盐水21天。第2组从第8天开始给予50mg/kg槲皮素21天。第3组在第0天给予10mg/kg硫酸博来霉素,并在第22天和第29天处死。第4组在第0天给药10mg/kg硫酸博来霉素,并给药50mg/kg槲皮素14天,从第8天开始给药21天。采用光镜、电镜、免疫组织化学和分子生物学方法对肺组织进行检查。损伤组显示肺泡结构受损,胶原积聚,肺泡间隔炎性细胞增加。槲皮素治疗可降低纤维反应,改善肺泡结构。与损伤组相比,损伤组的α-SMA表达较高,但治疗组的表达较低。与损伤组相比,损伤组E-钙粘蛋白表达降低,治疗组表现出更强的免疫反应性。miR-26b和miR-27b的表达在损伤组中低于对照组,在治疗组中高于损伤组。槲皮素可以被认为是特发性肺纤维化的一种新的治疗剂,因为它可以增加miR-26b和miR-27b的表达水平,从而降低纤维化,并对组织病理学变化具有治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Investigation of miR-26b and miR-27b expressions and the effect of quercetin on fibrosis in experimental pulmonary fibrosis

In this study, investigation of the effects of Quercetin on Bleomycin-induced pulmonary fibrosis and fibrosis-associated molecules miR-26b and miR-27b was aimed. Control group was given 10% saline on the 0th day, and saline was administered for 21 days starting from the 8th day. Group 2 was given 50 mg/kg Quercetin for 21 days starting from the 8th day. Group 3 was given 10 mg/kg Bleomycin Sulfate on day 0, and sacrificed on the 22nd and 29th day. Group 4 was given 10 mg/kg Bleomycin Sulfate on the 0th day, and was given 50 mg/kg Quercetin for 14 days, and 21 days starting from day 8. Lung tissues were examined using light and electron microscopic, immunohistochemical and molecular biological methods. Injury groups revealed impaired alveolar structure, collagen accumulation and increased inflammatory cells in interalveolar septum. Fibrotic response was decreased and the alveolar structure was improved with Quercetin treatment. α-SMA expressions were higher in the injury groups, but lower in the treatment groups compared to the injury groups. E-cadherin expressions were decreased in the injury groups and showed stronger immunoreactivity in the treatment groups compared to the injury groups. miR-26b and miR-27b expressions were lower in the injury groups than the control groups, and higher in the treatment groups than the injury groups. Quercetin can be considered as a new treatment agent in the idiopathic pulmonary fibrosis, since it increases the expression levels of miR-26b and miR-27b which decrease in fibrosis, and has therapeutic effects on the histopathological changes.

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来源期刊
Journal of Molecular Histology
Journal of Molecular Histology 生物-细胞生物学
CiteScore
5.90
自引率
0.00%
发文量
68
审稿时长
1 months
期刊介绍: The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.
期刊最新文献
Editorial: New perspectives from the new Editor-in-Chief of Journal of Molecular Histology. Correction: Dendrobine alleviates oleic acid-induced lipid accumulation by inhibiting FOS/METTL14 pathway. Correction: Zinc-alkaline phosphatase at sites of aortic calcification. PODXL promotes malignant progression of hepatocellular carcinoma by activating PI3K/AKT pathway. Biotoxicity of paraquat to lung cells mediated by endoplasmic reticulum-mitochondria interaction.
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