Network Pharmacology to Explore the Mechanism of Prunella vulgaris L. Against Prolactinoma

Author:

Meng Jun-Hua1,Ni Ping2,Cao Yu-Ling3,Zhang Yu2,Wang Xiong1,Zhang Hong4ORCID,Chen Yong-Gang1

Affiliation:

1. Department of Pharmacy, Wuhan University Tongren Hospital (The Third Hospital of Wuhan), Wuhan, Hubei, China

2. School of Pharmacy, Hubei University of Traditional Chinese Medicine, Wuhan, Hubei, China

3. Department of Pharmacy, Wuhan ASIA General Hospital, Wuhan, Hubei, China

4. Department of Pharmacy, The First People’s Hospital of Jiangxia District, Wuhan, Hubei, China

Abstract

Objectives Prolactinoma is a common intracranial tumor with a high incidence and serious harm to human health. At present, there is only one therapeutic drug in China, bromocriptine, and the Chinese herb Prunella vulgaris L. ( P. vulgaris)(PV) has shown certain anti-prolactinoma effects in the early stage. We expect to develop a candidate drug against prolactinoma. Materials and Methods First, the extracts of P. vulgaris L.(PVE)were extracted with water, and the cell proliferation test of rat pituitary tumor cells MMQ was checked by the Cell Counting Kit-8 (CCK-8) assay. Then, core targets and correlative pathways were selected by the “protein–protein interaction” (PPI) network and the “PV–Target–Prolactinoma” network. The core targets and main components simulate the binding by molecular docking. Finally, the PVE and MMQ cells were used to verify the results. Results Through the CCK-8 assay, the PVE inhibited the proliferation of MMQ cells. From the network pharmacology, the 21 targets, 9 signaling pathways, and 20 gene ontology (GO) projects were attained ( p < 0.05). As a result the estrogen receptor α (ESR1), RAC-alpha serine/threonine-protein kinase(AKT1), and mitogen-activated protein kinase 3(MAPK3)were the core targets of protein against prolactinomas, which was in line with western blotting analysis. Conclusion Our findings demonstrate that the PVE was verified against prolactinomas through the ESR1, MAPK3 targets, and the phosphoinositide 3-kinase/protein kinase B pathway.

Publisher

SAGE Publications

Subject

Drug Discovery,Pharmaceutical Science

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