Effect and mechanism of combined use of active components of Buyang Huanwu Decoction in ameliorating neuronal injury induced by OGD/R.
10.19540/j.cnki.cjcmm.20241115.502
- Author:
Cun-Yan DAN
1
;
Meng-Wei RONG
1
;
Xiu LOU
1
;
Tian-Qing XIA
1
;
Bao-Guo XIAO
2
;
Hong GUO
3
;
Cun-Gen MA
1
;
Li-Juan SONG
4
Author Information
1. Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine Jinzhong 030619, China.
2. State Key Laboratory of Neurobiology/Institute of Neurology,Fudan University Shanghai 200025, China.
3. State Key Laboratory of Component-based Chinese Medicine,Tianjin University of Traditional Chinese Medicine Tianjin 301617, China.
4. Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine Jinzhong 030619, China Ministry of Education Key Laboratory of Cell Physiology, Shanxi Medical University Taiyuan 030001, China.
- Publication Type:Journal Article
- Keywords:
Buyang Huanwu Decoction;
OGD/R;
amygdalin;
apoptosis;
cerebral schemic stroke;
hydroxysafflor yellow A;
neurons;
pyroptosis
- MeSH:
Drugs, Chinese Herbal/chemistry*;
Apoptosis/drug effects*;
Animals;
Neurons/cytology*;
Mice;
Molecular Docking Simulation;
Cell Line;
Glucose/metabolism*;
Humans;
Neuroprotective Agents/pharmacology*
- From:
China Journal of Chinese Materia Medica
2025;50(4):1098-1110
- CountryChina
- Language:Chinese
-
Abstract:
Buyang Huanwu Decoction(BYHWD), as one of the classic formulas in traditional Chinese medicine(TCM) for the treatment of cerebral ischemic stroke(CIS), has demonstrated definite effects in clinical practice. However, the material basis and mechanism of treatment have not been systematically elucidated. This study employed network pharmacology and molecular docking to analyze the potential targets and mechanisms of blood-and brain-penetrating active components of BYHWD in reducing cell apoptosis in CIS. Cell experiments were then carried out to validate the prediction results. In the experiments, five active components including hydroxysafflor yellow A( HSYA), tetramethylpyrazine( TMP), astragaloside Ⅳ( AS-Ⅳ), amygdalin( AMY), and paeoniflorin(PF) were selected to explore the pharmacological effects of BYHWD. HT22 cells were treated with BYHWD, and the cell counting kit-8(CCK-8) method was employed to examine the toxic and side effects of BYHWD. A cell model of oxygen-glucose deprivation/reoxygenation( OGD/R) was constructed, with apoptosis and pyroptosis as the main screening indicators. The levels of lactate dehydrogenase(LDH) and glutathione(GSH) were measured to assess the cell membrane integrity. Flow cytometry was employed to detect apoptosis, and the activities of caspase-3 and caspase-1 were measured to clarify the status of apoptosis and pyroptosis. ELISA was employed to determine the levels of interleukin(IL)-1β and IL-18 to confirm pyroptosis. HSYA and AMY were identified in this study as the active components regulating apoptosis and pyroptosis. TUNEL was employed to detect the apoptosis rate, and Western blot was employed to determine the expression levels of apoptosis-related proteins B-cell lymphoma-2(Bcl-2), Bcl-2-associated X protein(Bax), and caspase-3, which confirmed that the anti-apoptotic effect of the combined component group was superior to that of the single component groups. The molecular docking results revealed strong binding affinity of HSYA and AMY with SDF-1α and CXCR4.AMD3100, a selective antagonist of CXCR4, was then used for intervention. The results of Western blot showed alterations in the expression levels of apoptosis-associated proteins, SDF-1α, and CXCR4. In conclusion, HSYA and AMY influence cellular apoptosis by modulating the SDF-1α/CXCR4 signaling cascade.
