基于人工智能结合体内实验研究大柴胡汤治疗急性胰腺炎的作用机制。
Study on the Mechanism of Dachaihu Decoction in the Treatment of Acute Pancreatitis Based on Artificial Intelligence Combined with in vivo Experiments.
机构信息
Department of Respiratory and Gastroenterology, Xingtai First Hospital, Xingtai, Hebei, 054001, China.
出版信息
Comb Chem High Throughput Screen. 2023;26(13):2345-2357. doi: 10.2174/1386207326666230202140740.
BACKGROUND AND AIM
To explore the possible mechanism of Dachaihu Decoction (DCHD) in the treatment of AP, and use in vivo experiments to verify.
METHODS
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.
RESULTS
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 ( < 0.01), whereas CTNNB1 expression was found to be decreased in the model group ( < 0.01). Compared with the model group, the protein expression levels of EGFR, TNF, SRC, and VEGFA in the treatment group were down-regulated ( < 0.01), and CTNNB1 was up-regulated ( < 0.05).
CONCLUSION
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.
背景与目的
探讨大柴胡汤（DCHD）治疗急性胰腺炎（AP）的可能作用机制，并通过体内实验进行验证。
方法
采用网络药理学方法获取 DCHD 治疗 AP 的靶标和活性成分，并进行分子对接初步验证。使用缩胆囊素制备 AP 大鼠模型。通过 H&E 染色观察胰腺组织的变化。采用 Western blot 和 RT-qPCR 评估相关蛋白和 mRNA。
结果
网络药理学和分子对接结果显示，DCHD 治疗 AP 的关键靶标（EGFR、TNF、SRC、VEGFA 和 CTNNB1）和关键活性成分（β-谷甾醇、豆甾醇、黄芩素、槲皮素和山奈酚）具有良好的结合能力。H&E 染色显示，缩胆囊素干预后大鼠胰腺组织损伤明显，而 DCHD 可改善胰腺组织损伤。同时，与空白组相比，模型组 EGFR、TNF、SRC、VEGFA 蛋白和 mRNA 表达水平升高（<0.01），而 CTNNB1 表达水平降低（<0.01）。与模型组相比，治疗组 EGFR、TNF、SRC 和 VEGFA 蛋白表达水平下调（<0.01），CTNNB1 上调（<0.05）。
结论
DCHD 通过上调 CTNNB1 蛋白和 mRNA，同时抑制 EGFR、TNF、SRC 和 VEGFA 蛋白和 mRNA 表达，保护胰腺组织，改善 AP 大鼠症状。
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