Benzaldehyde stimulates autophagy via the sonic hedgehog signaling pathway in mouse brain astrocytes after treatment with Angiostrongylus cantonensis excretory-secretory products

Kuang Yao Chen*, Chien Ju Cheng, Yuan Ting Chang, Yi Hsuan Lin, Yi Hao Huang, Sheng Yu Lin, Lian Chen Wang, Kai Yuan Jhan, Cheng Hsun Chiu

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

摘要

Autophagy is a vital cellular process responsible for digesting various cytoplasmic organelles. This process plays a crucial role in maintaining cell survival and homeostasis, especially under conditions that cause nutrient deficiency, cellular damage, and oxidative stress. Neuroangiostrongyliasis is an infection caused by the parasitic nematode Angiostrongylus cantonensis and is considered as an emerging disease in many parts of the world. However, effective therapeutic strategies for neuroangiostrongyliasis still need to be further developed. In this study, we investigated the effects of benzaldehyde treatment on autophagy and sonic hedgehog (Shh) signaling in A. cantonensis-infected mice and its mechanisms. First, we found autophagosome generation in the central nervous system after A. cantonensis infection. Next, benzaldehyde combined with albendazole treatment reduced eosinophilic meningitis and upregulated the expression of Shh signaling- and autophagy-related molecules in A. cantonensis-infected mouse brains. In vitro experiments demonstrated that benzaldehyde could induce autophagy via the Shh signaling pathway in A. cantonensis excretory-secretory products (ESPs)-treated mouse astrocytes. Finally, benzaldehyde treatment also decreased lipid droplet accumulation and increased cholesterol production by activating the Shh pathway after ESPs treatment. In conclusion, these findings suggested that benzaldehyde treatment could alleviate brain damage by stimulating autophagy generation through the Shh signaling pathway.

原文英語
文章編號100560
頁(從 - 到)100560
期刊International Journal for Parasitology: Drugs and Drug Resistance
26
早期上線日期12 08 2024
DOIs
出版狀態已出版 - 12 2024

文獻附註

Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.

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