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Atractylenolide III Ameliorated Autophagy Dysfunction via EpidermalGrowth Factor Receptor-Mammalian Target of Rapamycin Signals and Alleviated Silicosis Fibrosis in Mice

ABSTRACT: Atractylenolide III Ameliorated Autophagy Dysfunction via EpidermalGrowth Factor Receptor-Mammalian Target of Rapamycin Signals and Alleviated Silicosis Fibrosis in Mice

PROVIDER: PRJNA1029521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26418427_1.fastq.gz	Fastqsanger.gz
	SRR26418427_2.fastq.gz	Fastqsanger.gz
	SRR26418428_1.fastq.gz	Fastqsanger.gz
	SRR26418428_2.fastq.gz	Fastqsanger.gz
	SRR26418429_1.fastq.gz	Fastqsanger.gz

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Atractylenolide III Ameliorated Autophagy Dysfunction via EpidermalGrowth Factor Receptor-Mammalian Target of Rapamycin Signals and Alleviated Silicosis Fibrosis in Mice

Project description:Atractylenolide III (ATL-III) is a major active constituent of the natural plant Atractylodes rhizome. Our previous study has shown that ATL-III may alleviate alveolar macrophage apoptosis via the inhibition of the mammalian target of rapamycin (mTOR)-mediated autophagy of human silicosis. Therefore, we aimed to further explore the function of ATL-III in autophagy, apoptosis, and pulmonary fibrosis by establishing the ATL-III-intervened silicosis mouse model in this study. Meanwhile, we sought and then verified potential autophagy-related signaling pathways by matching differentially expressed genes (attained by RNA sequencing) and the autophagy database. In this study, RNA-sequencing results implied that the epidermal growth factor receptor, the crucial upstream activator of mTOR, was seen as a potential autophagy-regulatory molecule in the ATL-IIIeintervened silicosis mouse model. The finding of this study was that ATL-III might improve the disorder of autophagic degradation via the activation of epidermal growth factor receptor-mTOR signals in the pulmonary tissue of the silicosis mouse model. ATL-III also alleviated cell apoptosis and silicotic fibrosis. Overall, we supposed that ATL-III might be a potential protective medicine, which had a regulatory effect on autophagy, for the intervention of silicotic fibrosis. In the future, the therapeutic drugs for silicosis should be further focused on the development and application of such natural autophagy agents.

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