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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 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Journal of Southern Medical University ›› 2026, Vol. 46 ›› Issue (7): 1543-1552.doi: 10.12122/j.issn.1673-4254.2026.07.08

Previous Articles    

Tongqiao Huoxue Decoction-medicated rat cerebrospinal fluid attenuates oxygen and glucose deprivation-induced neuronal injury by suppressing fibrinogen-mediated NLRP3 inflammasome activation

Yan WANG1(), Ping HUANG1, Yuqin PENG2, hao SUN2, Ning WANG2,3,4(), Changzhong WANG1()   

  1. 1.School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China
    2.School of Pharmacy, Anhui University of Chinese Medicine, Hefei 230012, China
    3.Anhui Provincial Key Laboratory of Research & Development of Chinese Medicine, Anhui University of Chinese Medicine, Hefei 230012, China
    4.Anhui Provincial Key Laboratory of Traditional Chinese Medicine Compounds, Anhui University of Chinese Medicine, Hefei 230012, China
  • Received:2025-11-26 Online:2026-07-20 Published:2026-07-20
  • Contact: Ning WANG, Changzhong WANG E-mail:yangwangsci@163.com;wnsci123@163.com;ahwcz63@sina.com

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Abstract:

Objective To examine the protective effects of cerebrospinal fluid from Tongqiao Huoxue Decoction-treated rats (TQHXD-CSF) against oxygen and glucose deprivation and reoxygenation (OGD/R)-induced injury in murine BV-2 microglial cells and co-cultured HT22 cells. Methods In a Transwell co-culture system of BV-2 and HT22 cells, OGD/R+fibrinogen (FIB) injury was induced in BV-2 cells followed by treatment with TQHXD-CSF intervention, and HT22 cells in the lower chamber were cultured under normal conditions. The cells were observed for changes in cell morphology, viability, intracellular ROS level, apoptosis, M1/M2 polarization, and FIB-containing extracellular vesicles (EVs). The cellular expressions of NLRP3, ASC, caspase-1, GSDMD, IL-1β, and IL-18 were quantified using Western blotting, and FIB-NLRP3 binding was confirmed by pull-down assay. Results OGD/R+FIB injury caused polarization of BV-2 cells to the pro-inflammatory M1 phenotype, increased CD86 expression and release of FIB-containing EVs, and activated the NLRP3 inflammasome. The co-cultured HT22 cells showed reduced cell viability, elevated ROS, and increased cells apoptosis. Treatment with TQHXD-CSF promoted M2 polarization in BV-2 cells, upregulated CD206 expression, suppressed FIB+ EVs secretion, and inhibited NLRP3 inflammasome activation in HT22 cells, which showed significantly lowered expressions of NLRP3, ASC, caspase-1, GSDMD, IL-1β, and IL-18 proteins and hence reduced inflammatory injury and cell apoptosis. Pull-down assay confirmed direct FIB and NLRP3 binding. Conclusion In the co-culture system of BV-2 cells and HT22 cells, TQHXD-CSF treatment protects HT22 cells against OGD/R+FIB-induced injury by inhibiting FIB-containing EVs release from BV-2 cells and suppressing NLRP3 inflammasome activation.

Key words: Tongqiao Huoxue Decoction, medicated cerebrospinal fluid, fibrinogen, NLRP3 inflammasome, extracellular vesicles