ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Amomum tsaoko Extract from Nujiang Alleviates DSS-Induced Colitis through Inhibiting Necroptosis
Provisionally accepted
Yuanyuan Wang1*
Keyi Lu1
Yuhang Gong1Yanna Shao1Siqi Liu1Yuan Fang2Yifan Shi1Erping Xu1Yanqiong Yang3Si Yuan3
Bai Ming1
Zhibin Wang4
Zhang Bo2- 1Henan University of Chinese Medicine, Zhengzhou, China
- 2Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai, China
- 3Nu jiang Lisu Autonomous Prefecture Traditional Chinese Medicine Hospital, Nujiang, China
- 4Naval Medical University, Shanghai, China
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Necroptosis, a form of programmed cell death, plays a significant role in compromising the intestinal barrier and initiating intestinal inflammation. An analysis of data from the Gene Expression Omnibus (GEO) reveals a strong correlation between ulcerative colitis (UC) and the pathological mechanisms of necroptosis. Consequently, inhibiting necroptosis may offer a promising strategy for ameliorating UC. Cao Guo (CG), a traditional Chinese medicine extensively utilized in China for both dietary and medicinal purposes, is frequently included in classical prescriptions for UC treatment. However, the precise chemical constituents of CG and its potential therapeutic targets for UC remain inadequately characterized. In this study, we analyzed the chemical composition of CG, employed a classic necroptosis model to assess the anti-necroptosis activity of CG, and conducted validation using a mouse model of UC. Through bioinformatics analysis and other methodologies, we initially explored the potential targets of CG in UC treatment and conducted subsequent verification. The findings demonstrate that in an in vitro necroptosis model, CG significantly enhances cell morphology and survival rates, while concurrently inhibiting the phosphorylation of RIPK1, RIPK3, and MLKL. In a mouse model of UC, CG alleviates weight loss and the disease activity index (DAI), ameliorates intestinal histopathological conditions, and upregulates the expression of tight junction proteins, such as ZO-1 and Occludin. Concurrently, CG diminishes the distribution and expression of phosphorylated RIPK3 and MLKL. Bioinformatics analysis suggests that CG may inhibit necroptosis via the signal transducer and activator of transcription 3 (STAT3) pathway, a hypothesis preliminarily validated through experimental methods. These results indicate that CG may exert therapeutic effects on UC by inhibiting STAT3 phosphorylation and suppressing necroptosis.
Keywords: Amomum tsaoko, Bioinformatics analysis, necroptosis, stat3, ulcerative colitis
Received: 17 Dec 2025; Accepted: 02 Feb 2026.
Copyright: © 2026 Wang, Lu, Gong, Shao, Liu, Fang, Shi, Xu, Yang, Yuan, Ming, Wang and Bo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuanyuan Wang
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