| Literature DB >> 31053932 |
Shizhang Wei1, Xuelin Zhou1, Ming Niu2, Haizhu Zhang3, Xiaoyi Liu2, Ruilin Wang4, Pengyan Li2, Haotian Li1, Huadan Cai1, Yanling Zhao5.
Abstract
Li-Ru-Kang (LRK) has been commonly used in the treatment of hyperplasia of mammary gland (HMG) as a cipher prescription and achieved obvious therapeutic effects. However, the bioactive compounds and underlying pharmacological mechanisms remain unclear. This study aims to decipher the bioactive compounds and potential action mechanisms of LRK in the treatment of HMG using an integrated pharmacology approach. The ingredients of LRK and the corresponding drug targets were retrieved through drug target databases and were used to construct the "compound-target-disease" network and function-pathway network. Ultimately, 89 compounds and 2150 drug targets were collected. Gene ontology enrichment analysis revealed that mammary gland alveolus development and mammary gland lobule development were the key biological processes and were regulated simultaneously by three direct targets, including androgen receptor (AR), estrogen receptor (ER) and cyclin-D1. Moreover, 14 compounds of LRK were directly involved in the regulation of the three aforementioned targets. KEGG pathway enrichment analysis found that five signaling pathways and seven direct targets were closely related with HMG treatment by LRK. The results of animal experiments showed that LRK significantly improved the histopathological status of HMG in rats. Additionally, LRK markedly regulated the protein expressions of AR, cyclin-D1, MMP2, MMP3 and MMP9. But interestingly, the effect of LRK on ER was not obvious. This study demonstrated that LRK exerted its therapeutic efficacy based on multi-components, multi-targets and multi-pathways. This research confirms the advantages of network pharmacology analyses and the necessity for experimental verification.Entities:
Keywords: Hyperplasia of mammary glands; Li-Ru-Kang; Mechanism of action; Network pharmacology
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Year: 2019 PMID: 31053932 DOI: 10.1007/s00438-019-01569-5
Source DB: PubMed Journal: Mol Genet Genomics ISSN: 1617-4623 Impact factor: 3.291