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青藤碱对大鼠肺动脉高压的治疗作用及其关键信号通路分析

陈子怡 黄小阳 曾振华 唐日红 吴卫华

药学研究2026,Vol.45Issue(7):729-733,751,6.
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药学研究2026,Vol.45Issue(7):729-733,751,6.DOI:10.13506/j.cnki.jpr.2026.07.002

青藤碱对大鼠肺动脉高压的治疗作用及其关键信号通路分析

The therapeutic effect of sinomenine on pulmonary arterial hypertension in rats and analysis of its key signaling pathways

陈子怡 1黄小阳 2曾振华 2唐日红 2吴卫华3

作者信息

  • 1. 徐州医科大学药学院,江苏 徐州 221004
  • 2. 湖南医药学院药学院,湖南 怀化 418000
  • 3. 徐州医科大学药学院,江苏 徐州 221004||湖南医药学院药学院,湖南 怀化 418000
  • 折叠

摘要

Abstract

Objective To explore the preventive and therapeutic effects of sinomenine(SIN)on monocrotaline(MCT)-induced pulmonary arterial hypertension(PAH)in rats,as well as its potential regulatory signaling pathways.Methods A rat model of PAH was established via MCT induction.Right heart catheterization was performed to measure the right ventricular systolic pressure(RVSP)in rats.High-throughput sequencing technology was used to analyze the gene expression profile of rat lung tissues,and enrichment analysis was employed to screen the key signaling pathways through which SIN ameliorates MCT-induced PAH in rats.Finally,quantitative real-time polymerase chain reaction(qRT-PCR)was utilized to detect the expression of core genes in the identified pathways.Results SIN significantly inhibited the MCT-induced increase in RVSP and thickness of pulmonary arterial vessels in rats.Analysis of lung tissue transcriptome data and detection of pulmonary arterial vascular genes revealed that SIN might ameliorate MCT-induced PAH in rats by inhibiting the extracellular matrix(ECM)-receptor interaction signaling pathway.Conclusion SIN may ameliorate MCT-induced PAH in rats by inhibiting the ECM-receptor interaction signaling pathway.

关键词

青藤碱/肺动脉高压/胞外基质/信号通路

Key words

Sinomenine/Pulmonary arterial hypertension/Extracellular matrix/Signaling pathway

分类

医药卫生

引用本文复制引用

陈子怡,黄小阳,曾振华,唐日红,吴卫华..青藤碱对大鼠肺动脉高压的治疗作用及其关键信号通路分析[J].药学研究,2026,45(7):729-733,751,6.

基金项目

湖南省自然科学基金区域联合项目(No.2025JJ70468) (No.2025JJ70468)

湖南省教育厅科学研究项目(No.23B1052、23A0720) (No.23B1052、23A0720)

药学研究

2095-5375

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