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橙皮苷通过调节EI24介导的自噬减轻肺纤维化。

Hesperidin alleviates pulmonary fibrosis by regulating EI24-mediated autophagy.

作者信息

Zhang Yan, Ma Wen, Wan Fang

机构信息

Department of Cadre's Ward, Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China.

Department of gerontology, Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China.

出版信息

Future Sci OA. 2025 Dec;11(1):2483147. doi: 10.1080/20565623.2025.2483147. Epub 2025 Mar 28.

DOI:10.1080/20565623.2025.2483147
PMID:40155367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11959899/
Abstract

BACKGROUND

Etoposide-induced protein 2.4 (EI24), an essential component of autophagy, is lowly expressed in pulmonary fibrosis. Hesperidin (Hes), a flavonoid, can regulate autophagy in various diseases. However, whether Hes can inhibit pulmonary fibrosis by mechanically regulating EI24-mediated autophagy has not been uncovered.

METHODS

RLE-6TN cells were treated with transforming growth factor β1 (TGF-β1) and rats were injected with bleomycin (BLM) to construct the pulmonary fibrosis model. The effect of Hes on pulmonary fibrosis was evaluated by cell counting kit-8, immunofluorescence, hematoxylin and eosin, masson trichome staining and western blotting.

RESULTS

Hes reduced cell viability of TGF-β1-induced RLE-6TN cells. Administration of Hes restored the decrease in autophagy marker levels in TGF-β1-induced RLE-6TN cells. Hes inhibited the transcriptional and translational levels of α-SMA, collagen I and fibronectin that were increased by TGF-β1 in RLE-6TN cells. Mechanically, Hes restored EI24 expression, and EI24 knockdown reversed the effect of Hes on the expressions of autophagy and fibrosis-related proteins. Additionally, Hes enhanced autophagy and fibrosis markers, which were worsened by EI24 knockdown in BLM-induced rats.

CONCLUSION

Hes activated autophagy by upregulating EI24, which improved pulmonary fibrosis both and .

摘要

背景

依托泊苷诱导蛋白2.4（EI24）是自噬的重要组成部分，在肺纤维化中低表达。橙皮苷（Hes）是一种黄酮类化合物，可调节多种疾病中的自噬。然而，Hes是否能通过机械调节EI24介导的自噬来抑制肺纤维化尚未明确。

方法

用转化生长因子β1（TGF-β1）处理RLE-6TN细胞，并用博来霉素（BLM）注射大鼠以构建肺纤维化模型。通过细胞计数试剂盒-8、免疫荧光、苏木精和伊红染色、Masson三色染色和蛋白质印迹法评估Hes对肺纤维化的影响。

结果

Hes降低了TGF-β1诱导的RLE-6TN细胞的活力。给予Hes可恢复TGF-β1诱导的RLE-6TN细胞中自噬标志物水平的降低。Hes抑制了TGF-β1在RLE-6TN细胞中诱导增加的α-SMA、胶原蛋白I和纤连蛋白的转录和翻译水平。从机制上讲，Hes恢复了EI24的表达，而EI24基因敲低逆转了Hes对自噬和纤维化相关蛋白表达的影响。此外，Hes增强了自噬和纤维化标志物，而在BLM诱导的大鼠中，EI24基因敲低使这些标志物恶化。

结论

Hes通过上调EI24激活自噬，从而改善肺纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/2bd06800faf1/IFSO_A_2483147_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/f48139261f25/IFSO_A_2483147_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/d0d557745f52/IFSO_A_2483147_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/17094f76d5da/IFSO_A_2483147_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/b434dd0a76d0/IFSO_A_2483147_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/d80392900eb9/IFSO_A_2483147_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/2bd06800faf1/IFSO_A_2483147_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/f48139261f25/IFSO_A_2483147_UF0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/d0d557745f52/IFSO_A_2483147_F0001_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/17094f76d5da/IFSO_A_2483147_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/b434dd0a76d0/IFSO_A_2483147_F0003_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/d80392900eb9/IFSO_A_2483147_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/11959899/2bd06800faf1/IFSO_A_2483147_F0005_C.jpg

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