111536
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
半夏泻心汤治疗溃疡性结肠炎的机制解析：靶向焦亡与坏死性凋亡
Authors Lu J, Liang K, Zhang L, Cui B , You L, An R, Hu C, Wang X
Received 9 September 2025
Accepted for publication 2 December 2025
Published 16 December 2025 Volume 2025:18 Pages 17537—17560
DOI https://doi.org/10.2147/JIR.S564333
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Nadia Andrea Andreani
Jie Lu,1,* Kun Liang,1,* Li Zhang,1 Bo Cui,1 Lisha You,1 Rui An,1 Cheng Hu,2 Xinhong Wang1
1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China; 2Innovation Center for Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xinhong Wang, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China, Email wangxinh6020@126.com Rui An, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China, Email anruimw@126.com
Purpose: Previous studies have highlighted a strong association between programmed cell death and ulcerative colitis (UC). Banxia Xiexin decoction (BXD) is a thoroughly validated formula with an extensive history of clinical application for treating UC. However, it remains unclear whether BXD regulates pyroptosis and necroptosis in UC. This study focused on pyroptosis and necroptosis to investigate the underlying mechanisms of BXD on UC.
Material and Methods: The therapeutic effects of BXD were evaluated in a dextran sulfate sodium (DSS)-induced colitis mouse model. To identify key signaling pathways, transcriptomics and proteomics were performed, followed by the validation of these pathways using Western blotting, immunohistochemistry, and immunofluorescence in vivo and in vitro. The bioactive components of BXD were screened through pharmacodynamic experiments, molecular docking, and surface plasmon resonance (SPR) analysis.
Results: BXD significantly alleviated UC symptoms by reducing inflammatory levels and improving intestinal barrier function. Multi-omics analyses demonstrated a significant alteration in pyroptosis- and necroptosis-related signaling pathways following BXD intervention. BXD suppressed pyroptosis through the P2RX7/NEK7 pathway and necroptosis via the TNFR1/RIPK3 pathway in the colons of UC model mice and in LPS+TNF-α-induced NCM460 cells. The screening of active ingredients revealed that baicalin and glycyrrhizic acid significantly affected LDH release and IL-1β levels. Molecular docking and SPR analyses demonstrated that baicalin targeted P2RX7 with high affinity and that glycyrrhizic acid targeted TNFR1 with moderate affinity.
Conclusion: BXD ameliorates inflammation and intestinal barrier dysfunction in UC by suppressing pyroptosis through the P2RX7/NEK7 pathway and necroptosis via the TNFR1/RIPK3 pathway. Baicalin and glycyrrhizic acid are identified as the pharmacodynamic components responsible for these therapeutic effects. These findings can provide molecular mechanisms and a material basis for the clinical application of BXD in the treatment of UC.
Keywords: ulcerative colitis, Banxia Xiexin decoction, multi-omics analyses, pyroptosis, necroptosis
1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China; 2Innovation Center for Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xinhong Wang, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China, Email wangxinh6020@126.com Rui An, School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, People’s Republic of China, Email anruimw@126.com
Purpose: Previous studies have highlighted a strong association between programmed cell death and ulcerative colitis (UC). Banxia Xiexin decoction (BXD) is a thoroughly validated formula with an extensive history of clinical application for treating UC. However, it remains unclear whether BXD regulates pyroptosis and necroptosis in UC. This study focused on pyroptosis and necroptosis to investigate the underlying mechanisms of BXD on UC.
Material and Methods: The therapeutic effects of BXD were evaluated in a dextran sulfate sodium (DSS)-induced colitis mouse model. To identify key signaling pathways, transcriptomics and proteomics were performed, followed by the validation of these pathways using Western blotting, immunohistochemistry, and immunofluorescence in vivo and in vitro. The bioactive components of BXD were screened through pharmacodynamic experiments, molecular docking, and surface plasmon resonance (SPR) analysis.
Results: BXD significantly alleviated UC symptoms by reducing inflammatory levels and improving intestinal barrier function. Multi-omics analyses demonstrated a significant alteration in pyroptosis- and necroptosis-related signaling pathways following BXD intervention. BXD suppressed pyroptosis through the P2RX7/NEK7 pathway and necroptosis via the TNFR1/RIPK3 pathway in the colons of UC model mice and in LPS+TNF-α-induced NCM460 cells. The screening of active ingredients revealed that baicalin and glycyrrhizic acid significantly affected LDH release and IL-1β levels. Molecular docking and SPR analyses demonstrated that baicalin targeted P2RX7 with high affinity and that glycyrrhizic acid targeted TNFR1 with moderate affinity.
Conclusion: BXD ameliorates inflammation and intestinal barrier dysfunction in UC by suppressing pyroptosis through the P2RX7/NEK7 pathway and necroptosis via the TNFR1/RIPK3 pathway. Baicalin and glycyrrhizic acid are identified as the pharmacodynamic components responsible for these therapeutic effects. These findings can provide molecular mechanisms and a material basis for the clinical application of BXD in the treatment of UC.
Keywords: ulcerative colitis, Banxia Xiexin decoction, multi-omics analyses, pyroptosis, necroptosis