Melatonin reduces lung injury in type 1 diabetic mice by the modulation of autophagy

IF 2.4 3区 生物学 Q4 CELL BIOLOGY BMC Molecular and Cell Biology Pub Date : 2024-03-14 DOI:10.1186/s12860-024-00505-9
Jafar Rezaie, Mojtaba Jahanghiri, Reza Mosaddeghi- Heris, Sina Hassannezhad, Nima Abdyazdani, Afshin Rahbarghazi, Mahdi Ahmadi
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Abstract

In recent years, the role of autophagy has been highlighted in the pathogenesis of diabetes and inflammatory lung diseases. In this study, using a diabetic model of mice, we investigated the expression of autophagy-related genes in the lung tissues following melatonin administration. Data showed histopathological remodeling in lung tissues of the D group coincided with an elevated level of IL-6, Becline-1, LC3, and P62 compared to the control group (p < 0.05). After melatonin treatment, histopathological remodeling was improved D + Mel group. In addition, expression levels of IL-6, Becline-1, LC3, and P62 were decreased in D + Mel compared to D group (P < 0.05). Statistically significant differences were not obtained between Mel group and C group (p > 0.05). Our results showed that melatonin injection can be effective in the amelioration of lung injury in diabetic mice presumably by modulating autophagy-related genes.
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褪黑激素通过调节自噬减轻1型糖尿病小鼠的肺损伤
近年来,自噬在糖尿病和肺部炎症性疾病发病机制中的作用日益突出。本研究利用糖尿病小鼠模型,研究了褪黑素给药后肺组织中自噬相关基因的表达。数据显示,与对照组相比,D 组肺部组织的组织病理学重塑与 IL-6、Becline-1、LC3 和 P62 水平的升高相吻合(P 0.05)。我们的研究结果表明,注射褪黑素可有效改善糖尿病小鼠的肺损伤,这可能是通过调节自噬相关基因实现的。
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来源期刊
BMC Molecular and Cell Biology
BMC Molecular and Cell Biology Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
5.50
自引率
0.00%
发文量
46
审稿时长
27 weeks
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