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jdk.nashorn.api.scripting.NashornScriptEngine.getInterface(java.lang.Object,java.lang.Class) public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.getInterface(java.lang.Class) public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.invokeMethod(java.lang.Object,java.lang.String,java.lang.Object[]) throws javax.script.ScriptException,java.lang.NoSuchMethodException public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.invokeFunction(java.lang.String,java.lang.Object[]) throws javax.script.ScriptException,java.lang.NoSuchMethodException public javax.script.Bindings jdk.nashorn.api.scripting.NashornScriptEngine.createBindings() public java.lang.Object javax.script.AbstractScriptEngine.get(java.lang.String) public void javax.script.AbstractScriptEngine.put(java.lang.String,java.lang.Object) public javax.script.ScriptContext javax.script.AbstractScriptEngine.getContext() public java.lang.Object javax.script.AbstractScriptEngine.eval(java.lang.String,javax.script.Bindings) throws javax.script.ScriptException public java.lang.Object javax.script.AbstractScriptEngine.eval(java.io.Reader) throws javax.script.ScriptException public java.lang.Object javax.script.AbstractScriptEngine.eval(java.lang.String) throws javax.script.ScriptException public java.lang.Object javax.script.AbstractScriptEngine.eval(java.io.Reader,javax.script.Bindings) throws javax.script.ScriptException public void javax.script.AbstractScriptEngine.setContext(javax.script.ScriptContext) public javax.script.Bindings javax.script.AbstractScriptEngine.getBindings(int) public void javax.script.AbstractScriptEngine.setBindings(javax.script.Bindings,int) public final void java.lang.Object.wait() throws java.lang.InterruptedException public final void java.lang.Object.wait(long,int) throws java.lang.InterruptedException public final native void java.lang.Object.wait(long) throws java.lang.InterruptedException public 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Journal of Southern Medical University ›› 2026, Vol. 46 ›› Issue (7): 1611-1621.doi: 10.12122/j.issn.1673-4254.2026.07.15

Previous Articles    

Rehmanniae radix preparata alleviates chronic kidney disease in mice through a multi-target mechanism

Zaoqiang LIN1(), Mengyao JIANG2, Liuchang FENG1, Kunyang FANG3, Pingjun FANG3, Qinxiang TAN1()   

  1. 1.Department of Nephrology, Shenzhen Hospital (Longgang), Beijing University of Chinese Medicine, Shenzhen 518116, China
    2.Department of Nephrology, Guangzhou University of Chinese Medicine, Guangzhou 510405, China
    3.Department of Hemodialysis, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China
  • Received:2025-10-15 Online:2026-07-20 Published:2026-07-20
  • Contact: Qinxiang TAN E-mail:13435683858@163.com;qinxiangtan2023@163.com

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Abstract:

Objective To explore the mechanisms of Rehmanniae radix preparate (RRP) for alleviating chronic kidney disease (CKD). Methods The active components and targets of RRP were identified using TCMSP and BATMAN-TCM databases. A component-target-pathway network was constructed, followed by GO and KEGG enrichment analyses. Molecular docking was performed between the core targets (JUN and STAT3) and the active compounds using AutoDock Vina. For validation of the results, C57BL/6 mice were randomly divided into sham-operated group, unilateral renal ischemia-reperfusion injury (UIRI) model group, and UIRI+RRP treatment group (n=6). RRP treatment was administered by daily gavage (300, 600 and 1200 mg·kg) from 2 days before to 10 days after surgery. On postoperative day 30, serum creatinine, uric acid, blood urea nitrogen, and urinary protein levels were analyzed, and renal histopathology was assessed using HE, Masson, and Sirius Red staining. Immunohistochemistry was used to detect renal expressions of JUN, STAT3, collagen I, and collagen III. Results A total of 25 active compounds and 307 CKD-related targets were identified, and protein-protein interaction analysis identified 19 hub genes with JUN and STAT3 as the key targets. Molecular docking showed strong binding affinities between the active compounds and JUN/STAT3. The mouse models of UIRI showed significant elevation of serum creatinine, uric acid, blood urea nitrogen, and urinary protein levels with marked tubular injury, interstitial fibrosis, and increased renal expressions of JUN, STAT3, collagen I, and collagen III. RRP treatment significantly reduced these biochemical parameters in the mouse models, improved renal histology, and downregulated JUN, STAT3, and fibrosis-related proteins. Conclusion The ameliorative effect of RRP against renal fibrosis and CKD progression in mice is mediated by a multi-component, multi-target, and multi-pathway mechanism targeting the JUN/STAT3 signaling pathway.

Key words: rehmanniae radix praeparata, chronic kidney disease, network pharmacology, JUN, STAT3