Title:Study on the Mechanism of Dachaihu Decoction in the Treatment of Acute
Pancreatitis Based on Artificial Intelligence Combined with in vivo Experiments
Volume: 26
Issue: 13
Author(s): Yan Zhang*, Sujie Li, Xiujiang Zhang, Pei Wang, Zhe Meng, Yuming Pang and Wei Li
Affiliation:
- Department of Respiratory and Gastroenterology, Xingtai First Hospital, Xingtai, Hebei, 054001, China
Keywords:
Acute pancreatitis, dachaihu decoction, molecular docking, network pharmacology, in vivo experiment, artificial intelligence.
Abstract:
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 (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).
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.
