Evidence map›Paper›PMID 41022599›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University

[Rosa laevigata Michx. inhibits pulmonary arterial smooth muscle cell proliferation in hypertension by modulating the Src-AKT1 axis].

Ziwei Yang, Chang Lü, Zhu Dong, Shulei Ji, Shenghui Bi, Xuehua Zhang, Xiaowu Wang

Abstract readEnglish Abstract
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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Ziwei YangDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Chang LüDepartment of Spinal Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Zhu DongDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Shulei JiDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Shenghui BiDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xuehua ZhangDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xiaowu WangDepartment of Cardiovascular Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.

Funding

Natural Science Foundation for the Youth (NSFY) of China 82300470
6 · The paper itself

Abstract

objectivesTo investigate the synergistic mechanism of the traditional Chinese medicine Rosa laevigata Michx. (RLM) for treatment of pulmonary arterial hypertension (PAH).

methodsNetwork pharmacological analysis was carried out to screen the active ingredients of RLM and PAH disease targets and construct the "component-target-disease" interaction network, followed by gene enrichment analysis and molecular docking studies. In the cell experiments, primary cultures of rat pulmonary arterial smooth muscle cells were exposed to hypoxia for 24 h and treated with solvent or 100, 200 and 300 mg/mL RLM, and the changes in cell proliferation were detected using Western blotting for PCNA and immunofluorescence staining. In the animal experiment, male SD rats were randomized into 5 control group, monocrotaline (MCT) solvent group, and MCT with RLM (100, 200 and 300 mg/mL) treatment groups. HE staining and immunofluorescence staining were used to observe histopathological changes in the pulmonary blood vessels of the rats.

resultsSeven core active ingredients (including β-sitosterol and kaempferol) in RLM and 39 key disease targets were identified, and molecular docking showed that SRC was a high-affinity target. KEGG enrichment analysis showed that the differential genes were significantly enriched in calcium signaling and PI3K-AKT pathways. In rat pulmonary arterial smooth muscle cells, hypoxic exposure significantly up-regulated cellular expression of PCNA and phosphorylation levels of Src and AKT1, which were obviously lowered by RLM treatment. In RLM-treated rat models, the mean pulmonary artery pressure and right ventricular hypertrophy index (Fulton index) were significantly reduced, the tricuspid annular plane systolic excursion (TAPSE) was improved, and pulmonary vascular wall thickening and fibrosis were obviously ameliorated.

conclusionsRLM inhibits pulmonary arterial smooth muscle cell proliferation in rat models of hypertension possibly by regulating the Src-AKT1 axis, suggesting the potential of RLM as a new natural drug for treatment of pulmonary hypertension.

Indexed as

Cell ProliferationDrugs, Chinese HerbalHypertension, PulmonaryMyocytes, Smooth MuscleProto-Oncogene Proteins c-aktAnimalsCells, CulturedMaleMuscle, Smooth, VascularPulmonary ArteryRatsRats, Sprague-DawleySignal Transductionsrc-Family KinasesDrugs, Chinese HerbalProto-Oncogene Proteins c-aktsrc-Family KinasesAKT1network pharmacologypulmonary hypertensionsmooth muscle cell proliferationSrc

Identifiers

PMID41022599
PMCPMC12479258

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.