Identification of key pharmacological components and targets for Aidi injection in the treatment of pancreatic cancer by UPLC-MS, network pharmacology, and in vivo experiments

• Published in: Chinese medicine Vol. 18; no. 1; pp. 7 - 14
• Main Authors: Wang, Haojia, Wu, Zhishan, Fan, Xiaotian, Wu, Chao, Lu, Shan, Geng, Libo, Stalin, Antony, Zhu, Yingli, Zhang, Fanqin, Huang, Jiaqi, Liu, Pengyun, Li, Huiying, You, Leiming, Wu, Jiarui
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 14.01.2023; BioMed Central; BMC
• Subjects: Aidi injection; Analysis; Cancer; Care and treatment; Liquid chromatography; Mass spectrometry; Molecular docking; Network pharmacology; Pancreatic cancer; Pharmacodynamic evaluation; Pharmacology; Tumor proteins; China; Network pharmacology; Aidi injection; Pharmacodynamic evaluation; Pancreatic cancer; Molecular docking
• ISSN: 1749-8546; 1749-8546
• DOI: 10.1186/s13020-023-00710-2

Pancreatic cancer is one of the most lethal cancers worldwide. Aidi injection (ADI) is a representative antitumor medication based on Chinese herbal injection, but its antitumor mechanisms are still poorly understood. In this work, the subcutaneous xenograft model of human pancreatic cancer cell line Panc-1 was established in nude mice to investigate the anticancer effect of ADI in vivo. We then determined the components of ADI using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS) and explored the possible molecular mechanisms against pancreatic cancer using network pharmacology. In vivo experiments, the volume, weight, and degree of histological abnormalities of implanted tumors were significantly lower in the medium and high concentration ADI injection groups than in the control group. Network pharmacology analysis identified four active components of ADI and seven key targets, TNF, VEGFA, HSP90AA1, MAPK14, CASP3, P53 and JUN. Molecular docking also revealed high affinity between the active components and the target proteins, including Astragaloside IV to P53 and VEGFA, Ginsenoside Rb1 to CASP3 and Formononetin to JUN. ADI could reduce the growth rate of tumor tissue and alleviate the structural abnormalities in tumor tissue. ADI is predicted to act on VEGFA, P53, CASP3, and JUN in ADI-mediated treatment of pancreatic cancer.