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苍术素调节ASAH3L以改善半乳糖代谢和炎症，从而减轻急性肺损伤。

Atractylodin modulates ASAH3L to improve galactose metabolism and inflammation to alleviate acute lung injury.

作者信息

Shi Kun, Xiao Yangxin, Qu Mumujiang, Xie Ying, Wang Yan, Ke Chang, Qu Linghang, Liu Yanju

机构信息

College of Pharmacy, Hubei University of Chinese Medicine, Wuhan 430065, China.

Center for Hubei TCM Processing Technology Engineering, Wuhan 430065, China.

出版信息

iScience. 2024 Aug 31;27(10):110751. doi: 10.1016/j.isci.2024.110751. eCollection 2024 Oct 18.

DOI:10.1016/j.isci.2024.110751
PMID:39351199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11440247/
Abstract

Acute lung injury (ALI) is a lung disease characterized by an excessive inflammatory response and damage to lung epithelial cells. Atractylodin (ATL) has good anti-inflammatory activity and protects the integrity of the epithelial cell barrier. However, the efficacy of ATL in the treatment of ALI and its mechanism is unclear. We investigated the efficacy of ATL in treating ALI and explored its targets and mechanisms. The results showed that ATL significantly reduced the wet-dry ratio of lungs of rats with ALI, improved the pathological changes, and lowered the expression of the inflammatory factors. Combined metabolomic and transcriptomic analyses showed that ATL can reduce inflammation by inhibiting and activating the HIF-1 signaling pathway and modulating ASAH3L to improve galactose metabolism, thereby alleviating ALI. In conclusion, ATL may be a potential drug for the treatment of acute lung injury.

摘要

急性肺损伤（ALI）是一种以过度炎症反应和肺上皮细胞损伤为特征的肺部疾病。苍术素（ATL）具有良好的抗炎活性，并能保护上皮细胞屏障的完整性。然而，ATL治疗ALI的疗效及其机制尚不清楚。我们研究了ATL治疗ALI的疗效，并探索了其靶点和机制。结果表明，ATL显著降低了ALI大鼠肺组织的湿干比，改善了病理变化，并降低了炎症因子的表达。代谢组学和转录组学联合分析表明，ATL可通过抑制和激活HIF-1信号通路以及调节ASAH3L来改善半乳糖代谢，从而减轻炎症，进而缓解ALI。总之，ATL可能是一种治疗急性肺损伤的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/029bd5dbba18/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/499237883094/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/f1bfe4917adc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/d6328b7cb669/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/62f7facdb197/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/d25c0d577770/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/e89957d3215b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/027cd510b652/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/b56c2d118e15/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/9d3ac1af360a/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/de026e93c480/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/029bd5dbba18/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/499237883094/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/f1bfe4917adc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/d6328b7cb669/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/62f7facdb197/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/d25c0d577770/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/e89957d3215b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/027cd510b652/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/b56c2d118e15/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/9d3ac1af360a/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/de026e93c480/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf24/11440247/029bd5dbba18/gr10.jpg

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