public javax.script.ScriptEngineManager() public javax.script.ScriptEngineManager(java.lang.ClassLoader) public javax.script.ScriptEngineManager() javax.script.ScriptEngineManager@44eb5bdd jdk.nashorn.api.scripting.NashornScriptEngine@6b81dee4 [Ljava.lang.reflect.Method;@1c26a009 public javax.script.CompiledScript jdk.nashorn.api.scripting.NashornScriptEngine.compile(java.lang.String) throws javax.script.ScriptException public javax.script.CompiledScript jdk.nashorn.api.scripting.NashornScriptEngine.compile(java.io.Reader) throws javax.script.ScriptException public javax.script.ScriptEngineFactory jdk.nashorn.api.scripting.NashornScriptEngine.getFactory() public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.eval(java.lang.String,javax.script.ScriptContext) throws javax.script.ScriptException public java.lang.Object jdk.nashorn.api.scripting.NashornScriptEngine.eval(java.io.Reader,javax.script.ScriptContext) throws javax.script.ScriptException public java.lang.Object 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 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Journal of Southern Medical University ›› 2026, Vol. 46 ›› Issue (8): 1936-1946.doi: 10.12122/j.issn.1673-4254.2026.08.21

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Xiaohe Granule improves breast hyperplasia in rats by promoting mammary epithelial cell apoptosis via activating the ASK1/MKK4/JNK signaling pathway

Yu ZHANG1(), Kang SUN1, Juda LIU1, Shuhan WANG1, Jing PEI2()   

  1. 1.Department of Thyroid and Breast Surgery, First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China
    2.Department of Breast Surgery, First Affiliated Hospital of Anhui Medical University, Hefei 230022, China
  • Received:2025-12-04 Online:2026-08-20 Published:2026-08-01
  • Contact: Jing PEI E-mail:doctorzhang0146@163.com;Peijing@ahmu.edu.cn

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Abstract:

Objective To explore the mechanism of Xiaohe Granule (XHG) for alleviating mammary hyperplasia in rats. Methods A non-pregnant female SD rat model of mammary hyperplasia was established by intramuscular injections of estradiol benzoate (0.5 mg/kg) and progesterone (5 mg/kg). With untreated rats as the control group, the rat models were treated with saline (model group) or low-, medium- or high-dose XHG daily gavage, or with high-dose XHG plus oral administration of GS-444217. After the treatments, nipple height, diameter, and uterine index of the rats were measured, and histological changes in the mammary tissue were observed with HE staining. The expressions of Ki-67 and caspase-3 protein in the mammary tissue were detected using immunohistochemistry, and mammary epithelial cell apoptosis was examined using TUNEL staining. Serum levels of E2, P, PRL, FSH, IL-1β, and TNF-α were detected using ELISA, and the expressions of ASK1/MKK4/JNK and apoptosis-related proteins were analyzed using RT-qPCR and Western blotting. Results Compared with the normal control rats, the rats in the model group showed significantly increased mammary diameter, nipple height, and uterine index with obvious acinar hyperplasia, ductal dilation, and inflammatory cell infiltration in the mammary tissue. The rat models also showed significantly increased Ki-67 expression and serum levels of E2, P, PRL, FSH, IL-1β and TNF-α, markedly increased Bcl-2 expression, and lowered protein levels of p-ASK1/ASK1, p-MKK4/MKK4, p-JNK/JNK, caspase-3, and Bax in the mammary tissue. Treatment with XHG significantly reversed these changes in a dose-dependent manner. Treatment with GS-444217 significantly attenuated the ameliorative effect of high-dose XHG on mammary hyperplasia in the rat models. Conclusion XHG alleviates mammary hyperplasia in rats by promoting apoptosis of hyperplastic mammary epithelial cells via activating the ASK1/MKK4/JNK signaling pathway.

Key words: mammary gland hyperplasia, Xiaohe Granule, cell apoptosis, ASK1/MKK4/JNK pathway, estrogen, progesterone