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Identification and validation of fecal complement component 3 and fibronectin as potential biomarkers for monitoring disease activity in ulcerative colitis based on a mouse model 认领 引用
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作者 Yangyun Guo Ziheng Yan +4 位作者 Jingyu Ye Ruifu Yang Yajun Song Hui Yue Yong Zhao 《Animal Models and Experimental Medicine》 CAS CSCD 2026年第7期1292-1301,共10页
Background:Ulcerative colitis(UC)is a typical inflammatory bowel disease requiring long-term management.Although fecal calprotectin(FC)is widely employed for assessing disease activity,it is still considered insuffici... Background:Ulcerative colitis(UC)is a typical inflammatory bowel disease requiring long-term management.Although fecal calprotectin(FC)is widely employed for assessing disease activity,it is still considered insufficient as a standalone tool.New biomarkers are needed to better predict risk and comprehensively reflect biological pathways.This study aimed to identify potential fecal biomarkers to monitor disease activity in UC.Methods:C57BL/6J mice were exposed to dextran sulfate sodium(DSS)treatment for 7 days.Feces were collected and subjected to proteomic analysis and enzyme-linked immunosorbent assay(ELISA).Mouse colon tissues were subjected to histopathological and immunofluorescence analyses.The correlations between the selected fecal proteins and disease severity were evaluated and compared with FC.Results:Proteomic analysis revealed increases in fecal complement component 3(C3)and fibronectin(FN)in the DSS group.Next,we measured fecal C3 and FN levels in mice using ELISA.Significant elevation in C3 and FN levels was observed as early as day 1 after DSS treatment,preceding the increase in FC.Both fecal C3 and FN demonstrated significant correlations with disease activity,with C3 exhibiting a stronger correlation than FC.Using immunofluorescence,we observed distinct C3 and FN expressions in both the colonic tissues and the intestinal lumen.Conclusion:These findings demonstrate that fecal C3 and FN are promising candidate biomarkers for monitoring UC disease activity,and their utility requires further validation in other colitis models and human cohorts. 展开更多
关键词 complement component 3(C3) disease activity fibronectin mouse model ulcerative colitis
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Niu Huang mitigates dextran sulfate sodium-induced colitis by modulating farnesoid X receptor activation and the complement 3/NLRP3 signaling pathway 认领 引用
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作者 Juan Shi Chong-Yang Ma +6 位作者 Xiao-Hui Zhang Kun-Jing Liu Jin-Ying Liu Qing-Guo Wang Xue-Qian Wang Fa-Feng Cheng Tian Xu 《World Journal of Gastroenterology》 SCIE CAS 2026年第17期135-155,共21页
BACKGROUND Ulcerative colitis(UC)is a chronic inflammatory bowel disease for which effective therapies are lacking.Niu Huang(NH)is a traditional Chinese medicine used for inflammatory disorders.However,its protective ... BACKGROUND Ulcerative colitis(UC)is a chronic inflammatory bowel disease for which effective therapies are lacking.Niu Huang(NH)is a traditional Chinese medicine used for inflammatory disorders.However,its protective effect on UC and its underlying mechanisms are unknown.AIM To uncover the mechanisms underlying the anti-colitis effects of the NH.METHODS Network pharmacology was applied to predict the active ingredients and targets of NH.Experimental validation was conducted in a dextran sulfate sodium-induced murine colitis model.The therapeutic efficacy was assessed using symptoms,histopathology,quantitative polymerase chain reaction,western blotting,immunohistochemistry and enzyme linked immunosorbent assay,while the underlying mechanism was investigated through integrated transcriptomic and proteomic analyses.In addition,the critical role of farnesoid X receptor(FXR)in mediating the effects of NH was validated using the FXR inhibitor guggulsterone and Fxr-/-mouse models.RESULTS Network pharmacology revealed that the bioactive component of NH is bile acid.Our animal experiments demonstrated that NH treatment significantly alleviated colitis symptoms and pathological damage.NH preserved intestinal mucosal integrity by upregulating occludin,claudin3,E-cadherin and leucine rich repeat containing G protein-coupled receptor 5 expression.Transcriptomic and proteomic analyses revealed that bile secretion,the nuclear factor kappa B signaling pathway and the complement and coagulation cascade pathway are key targets of NH.Western blotting confirmed that NH increased FXR levels and reduced P65,complement component 3(C3)and NOD-like receptor family pyrin domain containing 3(NLRP3)expression.Furthermore,experiments using Fxr-/-mice and the FXR antagonist revealed that FXR is a pivotal target through which NH attenuates UC.Mechanistic analysis revealed that the effects of NH on UC are mediated by the modulation of targets involved in the activation of FXR and the subsequent inhibition of C3/NLRP3 activation.CONCLUSION This study demonstrates the therapeutic effects of NH on UC.Mechanistically,NH acts by activating FXR,which subsequently inhibits the nuclear factor kappa B pathway to reduce C3 accumulation and suppress excessive NLRP3 inflammasome activation in colon tissue. 展开更多
关键词 Niu Huang Ulcerative colitis Network pharmacology Farnesoid X receptor Complement component 3/NOD-like receptor family pyrin domain containing 3 signaling pathway Inflammation
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