褪黑素通过调节自噬减少 1 型糖尿病小鼠的肺损伤。

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

机构信息

Solid Tumor Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran.

Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

BMC Mol Cell Biol. 2024 Mar 14;25(1):7. doi: 10.1186/s12860-024-00505-9.

BACKGROUND

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.

RESULTS

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).

CONCLUSION

Our results showed that melatonin injection can be effective in the amelioration of lung injury in diabetic mice presumably by modulating autophagy-related genes.

背景

近年来，自噬在糖尿病和炎症性肺病的发病机制中的作用已得到强调。在这项研究中，我们使用糖尿病小鼠模型，研究了褪黑素给药后肺组织中与自噬相关的基因表达。

结果

数据显示，与对照组相比，D 组的肺组织存在组织病理学重塑，同时 IL-6、Becline-1、LC3 和 P62 水平升高（p<0.05）。褪黑素治疗后，D+Mel 组的组织病理学重塑得到改善。此外，与 D 组相比，D+Mel 组的 IL-6、Becline-1、LC3 和 P62 表达水平降低（P<0.05）。Mel 组和 C 组之间未获得统计学显著差异（p>0.05）。