Current pharmaceutical design · 2026
Exploring Key Target Genes of Tong Bian Bai Tou Weng Decoction for Ulcerative Colitis: A Combined Approach of Mendelian Randomization, Network Pharmacology, and Transcriptomics.
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Cui Can, Jiang Jia-Qi, Li Zhi-Cheng, Yin Xiang-Yi, Lu Yu-Chang, Wang Zhen-Yi
Аннотация
INTRODUCTION: Ulcerative colitis (UC) manifests as persistent inflammation and ulceration within the mucosal and submucosal layers of the colon. The present study sought to elucidate the principal targets of Tongbian Baitouweng Decoction (TBD) in UC.
METHODS: A total of 221 TBD-related and 1,270 UC-related genes were retrieved from public databases, with their intersection as candidate targets. Differential expression, machine learning, expression profiling, MR analysis, network construction, molecular docking, enrichment, and immune infiltration analyses were used to refine key targets and explore their functional associations with UC.
RESULTS: PPARG, STAT1, and IL1B emerged as the principal targets of TBD against UC. Among UC samples, IL1B and STAT1 were upregulated, whereas PPARG was downregulated. MR analysis revealed significant causal associations: STAT1 (OR = 1.17), IL1B (OR = 0.50), and PPARG (OR = 0.97). A network comprising three targets and 53 corresponding active compounds was established, with molecular docking demonstrating strong binding affinities, particularly with quercetin. Enrichment analysis indicated that the three targets were jointly involved in pathways such as "Toll-like receptor signaling". Immune infiltration analysis revealed that IL1B and STAT1 correlated positively with activated CD4 T cells, macrophages, and natural killer cells, whereas PPARG displayed an inverse pattern.
DISCUSSION: These findings align with existing evidence linking STAT1, PPARG, and IL1B to UC pathogenesis, highlighting TBD's therapeutic potential by targeting key inflammatory and barrier-regulatory pathways; future studies should validate these targets in preclinical models and explore the formula's clinical efficacy in large-scale trials.
CONCLUSION: STAT1, PPARG, and IL1B were TBD's key UC therapeutic targets, with regulatory roles providing a UC research mechanistic framework.
METHODS: A total of 221 TBD-related and 1,270 UC-related genes were retrieved from public databases, with their intersection as candidate targets. Differential expression, machine learning, expression profiling, MR analysis, network construction, molecular docking, enrichment, and immune infiltration analyses were used to refine key targets and explore their functional associations with UC.
RESULTS: PPARG, STAT1, and IL1B emerged as the principal targets of TBD against UC. Among UC samples, IL1B and STAT1 were upregulated, whereas PPARG was downregulated. MR analysis revealed significant causal associations: STAT1 (OR = 1.17), IL1B (OR = 0.50), and PPARG (OR = 0.97). A network comprising three targets and 53 corresponding active compounds was established, with molecular docking demonstrating strong binding affinities, particularly with quercetin. Enrichment analysis indicated that the three targets were jointly involved in pathways such as "Toll-like receptor signaling". Immune infiltration analysis revealed that IL1B and STAT1 correlated positively with activated CD4 T cells, macrophages, and natural killer cells, whereas PPARG displayed an inverse pattern.
DISCUSSION: These findings align with existing evidence linking STAT1, PPARG, and IL1B to UC pathogenesis, highlighting TBD's therapeutic potential by targeting key inflammatory and barrier-regulatory pathways; future studies should validate these targets in preclinical models and explore the formula's clinical efficacy in large-scale trials.
CONCLUSION: STAT1, PPARG, and IL1B were TBD's key UC therapeutic targets, with regulatory roles providing a UC research mechanistic framework.