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首页|期刊导航|医药导报|基于PI3K/AKT/mTOR信号通路探讨金匮肾气丸治疗慢性肾脏病血管钙化的机制

基于PI3K/AKT/mTOR信号通路探讨金匮肾气丸治疗慢性肾脏病血管钙化的机制

徐丽 谢欣昇 李勇 周鹏 曲鑫鑫 孙妲男

医药导报2026,Vol.45Issue(3):410-415,6.
医药导报2026,Vol.45Issue(3):410-415,6.DOI:10.3870/j.issn.1004-0781.2026.03.008

基于PI3K/AKT/mTOR信号通路探讨金匮肾气丸治疗慢性肾脏病血管钙化的机制

Mechanism of Jinkui Shenqi Pill in Treating Vascular Calcification in Chronic Kidney Disease via the PI3K/AKT/mTOR Signaling Pathway

徐丽 1谢欣昇 2李勇 1周鹏 3曲鑫鑫 1孙妲男1

作者信息

  • 1. 黑龙江中医药大学附属第二医院肾病科,哈尔滨 150040
  • 2. 黑龙江中医药大学附属第二医院骨伤一科,哈尔滨 150040
  • 3. 黑龙江中医药大学研究生院,哈尔滨 150040
  • 折叠

摘要

Abstract

Objective To investigate the mechanism of Jinkui Shenqi pill(JKSQ)in alleviating vascular calcification in chronic kidney disease(CKD)via the Phosphatidylinositol 3-kinase(PI3K)/Protein Kinase B(AKT)/Mammalian Target of Rapamycin(mTOR)signaling pathway.Methods A rat model of CKD with vascular calcification was established by intragas-tric administration of adenine combined with a high-phosphorus diet for 6 weeks.SD rats were randomly divided into six groups:control group,model group,calcitriol group,and JKSQ high-,medium-,and low-dose groups(n=12 per group).After successful modeling,the groups received respective interventions for 4 weeks:the model and control groups received an equal volume of nor-mal saline;the treatment groups received high-,medium-,or low-dose JKSQ or calcitriol via gavage.Serum levels of creatinine(Cr),urea nitrogen(BUN),phosphorus,and tissue calcium were measured.Pathological changes in the abdominal aorta were ob-served,and the expression of key proteins in the PI3K/AKT/mTOR signaling pathway was detected.Results Compared with the control group,the model group showed significantly increased serum Cr,BUN,phosphorus,tissue calcium levels,and the for-mation of abdominal aortic calcified plaques,indicating successful modeling.JSP treatment dose-dependently ameliorated these in-dicators and alleviated vascular calcification.The medium-and high-dose JKSQ groups showed significantly superior effects com-pared to the low-dose group.Notably,the high-dose JKSQ group was comparable to the calcitriol group in reducing Cr levels,whereas calcitriol had no significant effect on serum phosphorus and tissue calcium.Mechanistic studies revealed that JKSQ dose-dependently up-regulated the protein expression of PI3K,p-AKT,and p-mTOR in the abdominal aorta.Conclusion JKSQ may alleviate vascular calcification in chronic kidney disease by activating the PI3K/AKT/mTOR signaling pathway.

关键词

金匮肾气丸/慢性肾脏病/PI3K/AKT/mTOR信号通路/血管钙化

Key words

Jinkui Shenqi pill/Chronic kidney disease/PI3K/AKT/mTOR signaling pathway/Vascular calcification

分类

医药卫生

引用本文复制引用

徐丽,谢欣昇,李勇,周鹏,曲鑫鑫,孙妲男..基于PI3K/AKT/mTOR信号通路探讨金匮肾气丸治疗慢性肾脏病血管钙化的机制[J].医药导报,2026,45(3):410-415,6.

基金项目

黑龙江省自然科学基金项目(LH2021H086) (LH2021H086)

黑龙江省中医药科研项目(ZHY2020-139,ZHY2022-176) (ZHY2020-139,ZHY2022-176)

黑龙江省博士后研究人员落户黑龙江科研启动金资助项目(LBH-Q21190). (LBH-Q21190)

医药导报

1004-0781

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