Jiawei Foshou San Induces Apoptosis in Ectopic Endometrium Based on Systems Pharmacology, Molecular Docking, and Experimental Evidence

Jiahui Wei; Binxin Zhao; Chengling Zhang; Bingbing Shen; Ying Zhang; Changxi Li; Yi Chen

doi:10.1155/2019/2360367

Jiawei Foshou San Induces Apoptosis in Ectopic Endometrium Based on Systems Pharmacology, Molecular Docking, and Experimental Evidence

Evid Based Complement Alternat Med. 2019 Oct 27:2019:2360367. doi: 10.1155/2019/2360367. eCollection 2019.

Authors

Jiahui Wei^{1

2

3

4}, Binxin Zhao^{1

2

3

4}, Chengling Zhang^{1

2

3

4}, Bingbing Shen⁵, Ying Zhang^{1

2

3

4}, Changxi Li⁶, Yi Chen^{1

2

3

4}

Affiliations

¹ College of Pharmaceutical Sciences & Chinese Medicine, Southwest University, Chongqing, China.
² Chongqing Key Laboratory of New Drug Screening from Traditional Chinese Medicine, Chongqing, China.
³ Pharmacology of Chinese Materia Medica-the Key Discipline Constructed by the State Administration of Traditional, Chinese Medicine, Chongqing, China.
⁴ National Demonstration Center for Experimental Pharmacy Education (Southwest University), Chongqing, China.
⁵ The First Affiliated Hospital to Army Medical University, Chongqing 400038, China.
⁶ Department of Anesthesia, Chongqing Public Health Medical Center, Chongqing, China.

Abstract

Foshou San is a typical gynaecological formula with wild usage in traditional Chinese medicine. Jiawei Foshou San (JFS) is a novel ingredient prescription from Foshou San with antiendometriosis effect in unclear mechanisms. To uncover the potential application and proapoptotic mechanisms of JFS, JFS ingredient-drug target-disease networks, GO enrichment, and pathway analysis were established for potential application prediction. Molecular docking and validation in vivo were investigated by the proapoptotic mechanisms of JFS. In this study, 99 common targets were related to 108 diseases. 484 biological processes, 44 cell components, 59 molecular functions, and 37 pathways were significantly identified in GO enrichment and pathway analysis. In molecular docking, ligustrazine showed binding activity with Bcl-2, Bax, caspase-9, caspase-3, and PARP. In vivo, JFS elevated the shrink rate of ectopic endometrium, by suppressing E2 and PROG. An in-depth study showed that apoptosis was activated through diminishing Bcl-2, rising Bax and Bad, and expressing more caspase-3 and caspase-9 using JFS. JFS promoted the protein level of cleaved-PARP. In brief, JFS might be applied for various diseases through multiple targets and pathways, especially endometriosis by Bcl-2 pathway. These findings reveal the potential application for further evaluation and uncover the proapoptotic mechanism of JFS.