ArticleJournal of traditional and complementary medicine2025
Integrated serum pharmacochemistry and network pharmacology to reveal the kernel material basis and underlying mechanisms of the fuzi-lizhong pill for ulcerative colitis.
Article in Journal of traditional and complementary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Targeting the Gut Microbiota with Herbal Compounds from Traditional Chinese Medicine: A Mechanistic Synthesis of a Novel Therapeutic Approach for Ulcerative Colitis.Journal of inflammation research · 2026Review
- Unveiling Yiyi Fuzi Baijiang powder: Microecological and network pharmacology approach to ulcerative colitis treatment.World journal of gastroenterology · 2025Article
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Authors and funding
9 authors.
Funding
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Abstract
Background: In traditional Chinese medicine, Fuzi-Lizhong pill (FLZP) has been used for millennia as a treatment for the Spleen-Kidney-Yang-deficiency (SKYD) diseases. FLZP has increasingly been employed in the clinic as a therapeutic option for ulcerative colitis with SKYD syndrome (SKYD-UC). In the present study, we revealed the kernel material basis and underlying mechanisms of the FLZP for treating SKYD-UC. Methods and results: The therapeutic effects of FLZP were assessed in SKYD-UC rats. In total, 55 absorbed components of FLZP were identified, thus forming the main material basis for the use of FLZP for treating SKYD-UC. Network pharmacology analyses revealed that the ability of FLZP to exert multi-target synergistic activity was found to be related to both antioxidant and anti-inflammatory activity. More specifically, FLZP was suggested to alleviate SKYD-UC through the regulation of targets associated with inflammation such as interleukin-6 (IL-6), myeloperoxidase (MPO), and tumor necrosis factor-α (TNF-α), while also regulating the mitogen-activated protein kinase (MAPK), TNF, and phosphoinositol-3 kinase-RAC-alpha serine/threonine-protein kinase (PI3K-Akt) pathways. Ultimately, the integration of network analyses, molecular docking studies, and Pearson correlation analyses enabled the identification of 9 core compounds (including linolenic acid, liquirtigenin, 7-hydroxycoumarin, glycyrrhizic acid, 6-shogaol, dehydro-10-gingerdione, caffeic acid, 6-gingerol, liquiritin), which can serve as kernel material basis for FLZP in the treatment of SKYD-UC. Conclusion: Together, these findings offer a valuable foundation for additional research focused on the mechanistic effects and broader clinical application of FLZP as a treatment option for SKYD-UC.
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