4.7 Article

Protective effect of astragalus membranaceus and its bioactive compounds against the intestinal inflammation in Drosophila

期刊

FRONTIERS IN PHARMACOLOGY
卷 13, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2022.1019594

关键词

inflammatory bowel disease; Astragalus membranaceus; intestinal homeostasis; bioactive compounds; Drosophila melanogaster

资金

  1. National Natural Science Foundation of China
  2. Gansu Planning Projects on Science and Technology [82104562, 82004228]
  3. Scientific Research and Cultivation Project of Basic Disciplines of Integrated Chinese and Western Medicine [20JR10RA332]
  4. Pharmaceutical Research project of Gansu Provincial Drug Administration [ZXYJHJC-2020-02]
  5. [2022GSMPA004]

向作者/读者索取更多资源

Astragalus membranaceus extract (AME) provides protection against sodium dodecyl sulfate (SDS)-induced colitis in Drosophila flies by suppressing oxidative stress-associated JNK and JAK-STAT signaling pathways, offering a potential natural medicine for intestinal inflammatory disease in humans.
Inflammatory bowel disease (IBD) is characterized by chronic and relapsing intestinal inflammation, which currently lacks safe and effective medicines. Astragalus membranaceus (AM), also named Huangqi, is one of the most commonly used fundamental herbs in China. Here, we aimed to investigate mechanism and bioactive compounds of AM on treating sodium dodecyl sulfate (SDS)-induced colitis in Drosophila flies. Our data showed that AM extract (AME) supplementation had no toxic effect in flies, and protected flies against SDS-induced lifespan shortening, intestinal morphological damage, and colon length shortening. Moreover, AME supplementation remarkably rescued SDS-induced intestinal stem cell (ISC) overproliferation and increased reactive oxygen species (ROS) level in the intestine. Mechanistically, AME remarkably rescued the altered expression levels of genes and proteins in c-Jun N-terminal kinase (JNK) and JAK-STAT signaling pathways induced by SDS in gut. Additionally, formononetin, isoliquiritigenin, isorhamnetin, astragaloside I, astragaloside III, vanillic acid, and caffeic acid in AM had protection against SDS-induced inflammatory damage in flies. Taken together, AME could ameliorate the intestinal inflammation partially by suppressing oxidative stress-associated JNK signaling and JAK-STAT signaling pathways. AME may provide a theoretical basis for natural medicine toward treating intestinal inflammatory disease in human.

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