Study on the Mechanism of Dachaihu Decoction in the Treatment of Acute Pancreatitis Based on Artificial Intelligence Combined with in vivo Experiments

体内 免疫印迹 信使核糖核酸 汤剂 药理学 山奈酚 血管内皮生长因子A 化学 血管内皮生长因子 医学 槲皮素 血管内皮生长因子受体 癌症研究 生物 内科学 生物化学 生物技术 基因 抗氧化剂
作者
Yan Zhang,Sujie Li,Xiujiang Zhang,Pei Wang,Zhe Meng,Yuming Pang,Wei Li
出处
期刊:Combinatorial Chemistry & High Throughput Screening [Bentham Science]
卷期号:26 (13): 2345-2357
标识
DOI:10.2174/1386207326666230202140740
摘要

To explore the possible mechanism of Dachaihu Decoction (DCHD) in the treatment of AP, and use in vivo experiments to verify.The targets and active ingredients of DCHD in the treatment of AP were obtained through network pharmacology, and the preliminary verification was carried out by molecular docking. Caerulein was used to develop the AP rat model. H&E staining was performed to observe variations in pancreatic tissue. Western blot and RT-qPCR were conducted to evaluate the associated proteins and mRNA.The network pharmacology and molecular docking results showed that the key targets (EGFR, TNF, SRC, VEGFA and CTNNB1) and key active components (beta-sitosterol, stigmasterol, baicalein, quercetin, and kaempferol) of DCHD in the treatment of AP had good binding. H&E staining revealed that rat pancreatic tissues considerably damaged post caerulein intervention, and it has also been suggested that DCHD ameliorates damage to pancreatic tissue. Simultaneously, EGFR, TNF, SRC, VEGFA protein, and mRNA expression levels were increased in the model group compared to the blank group (P < 0.01), whereas CTNNB1 expression was found to be decreased in the model group (P < 0.01). Compared with the model group, the protein expression levels of EGFR, TNF, SRC, and VEGFA in the treatment group were down-regulated (P < 0.01), and CTNNB1 was up-regulated (P < 0.05).DCHD protects pancreatic tissues and improves symptoms in AP rats by upregulating CTNNB1 protein and mRNA while inhibiting EGFR, TNF, SRC, and VEGFA protein and mRNA expression.
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