Biochemistry and biophysics reports · 2026
A comparative study of dextran sodium sulfate-induced and spleen-kidney syndrome-based ulcerative colitis models.
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Yang Shasha, Xie Fuyu, Lin Xia, Zhang Yue, Wang Yue, Huang You, Zhang Xing, Hao Yiwen, Zhou Hang, Fu Chaomei, Tang Zhishu, Zhang Zhen
Аннотация
OBJECTIVE: Accurate animal models are essential for elucidating the pathogenesis of ulcerative colitis (UC). The widely used dextran sodium sulfate-induced UC (DSS-UC) model inadequately reflects the refractory nature of human UC. This study compared the traditional Chinese medicine (TCM)-based SKYD-UC model with the DSS-UC model to identify a more representative model.
METHODS: Network pharmacology was used to analyze the fundamental TCM syndrome of UC and to identify differential targets and pathways between DSS-UC and SKYD-UC. Both UC animal models were subsequently established, and body weight, organ indices, disease activity index (DAI) scores, colon length, mucosal damage, and serum biomarkers (IL-6, TNF-α, MPO, GSH-Px, GAS, and MTL) were evaluated.
RESULTS: Among the seven TCM syndromes, SKYD-UC presented the greatest number of targets and pathways, highlighting its fundamental importance. Specifically, 464 and 703 unique targets were identified for DSS-UC and SKYD-UC, respectively. DSS-UC unique targets were predominantly associated with inflammation, immune regulation, and cellular signaling. In contrast, SKYD-UC targets encompass a broader range of biological processes, including mitochondrial dysfunction, extracellular matrix remodeling, and pathways related to systemic UC complications. These findings were validated in animal experiments. Compared with the DSS-UC model, the SKYD-UC model demonstrated more severe damage, including pronounced spleen and thymus atrophy (p < 0.01), higher DAI scores (p < 0.01), shorter colons (p < 0.05), worse inflammation (elevated IL-6 and MPO) and gastrointestinal dysfunction (reduced GAS and elevated MTL) (p < 0.01), and unique kidney yang deficiency damage (elevated kidney index, p < 0.01), along with sustained weight loss.
CONCLUSION: While both models reflect inflammation and immune dysregulation, the SKYD-UC model better simulates the refractory nature of UC, offering an effective animal model for UC research.
METHODS: Network pharmacology was used to analyze the fundamental TCM syndrome of UC and to identify differential targets and pathways between DSS-UC and SKYD-UC. Both UC animal models were subsequently established, and body weight, organ indices, disease activity index (DAI) scores, colon length, mucosal damage, and serum biomarkers (IL-6, TNF-α, MPO, GSH-Px, GAS, and MTL) were evaluated.
RESULTS: Among the seven TCM syndromes, SKYD-UC presented the greatest number of targets and pathways, highlighting its fundamental importance. Specifically, 464 and 703 unique targets were identified for DSS-UC and SKYD-UC, respectively. DSS-UC unique targets were predominantly associated with inflammation, immune regulation, and cellular signaling. In contrast, SKYD-UC targets encompass a broader range of biological processes, including mitochondrial dysfunction, extracellular matrix remodeling, and pathways related to systemic UC complications. These findings were validated in animal experiments. Compared with the DSS-UC model, the SKYD-UC model demonstrated more severe damage, including pronounced spleen and thymus atrophy (p < 0.01), higher DAI scores (p < 0.01), shorter colons (p < 0.05), worse inflammation (elevated IL-6 and MPO) and gastrointestinal dysfunction (reduced GAS and elevated MTL) (p < 0.01), and unique kidney yang deficiency damage (elevated kidney index, p < 0.01), along with sustained weight loss.
CONCLUSION: While both models reflect inflammation and immune dysregulation, the SKYD-UC model better simulates the refractory nature of UC, offering an effective animal model for UC research.