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

IF 0.6 4区 医学 Q4 CHEMISTRY, MEDICINAL
Jun-Hua Meng, Ping Ni, Yu-Ling Cao, Yu Zhang, Xiong Wang, Hong Zhang, Yong-Gang Chen
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引用次数: 0

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 < .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.
网络药理学探讨夏枯草抗催乳素瘤的作用机制
目的催乳素瘤是一种常见的颅内肿瘤,发病率高,严重危害人体健康。目前国内只有溴隐亭一种治疗药物,中草药夏枯草(Prunella vulgaris L., P. vulgaris)(PV)在早期表现出一定的抗催乳素瘤作用。我们希望开发一种抗催乳素瘤的候选药物。材料与方法首先用水提取寻常草提取物(PVE),采用细胞计数试剂盒-8 (CCK-8)法检测大鼠垂体瘤细胞MMQ的细胞增殖试验。然后,通过“蛋白-蛋白相互作用”(protein-protein interaction, PPI)网络和“PV-Target-Prolactinoma”网络选择核心靶点和相关通路。核心靶点和主要组分模拟分子对接结合。最后,用PVE和MMQ细胞验证结果。结果通过CCK-8实验,PVE能抑制MMQ细胞的增殖。网络药理学共获得21个靶点、9个信号通路和20个基因本体(GO)项目(p <. 05)。结果表明,雌激素受体α (ESR1)、rac - α丝氨酸/苏氨酸蛋白激酶(AKT1)和丝裂原活化蛋白激酶3(MAPK3)是抗催乳素瘤蛋白的核心靶点,与western blotting分析结果一致。结论PVE可通过ESR1、MAPK3靶点和磷酸肌肽3-激酶/蛋白激酶B途径抑制催乳素瘤。
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来源期刊
Pharmacognosy Magazine
Pharmacognosy Magazine CHEMISTRY, MEDICINAL-
CiteScore
1.87
自引率
0.00%
发文量
37
审稿时长
3 months
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