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Buyang Huanwu Decoction Alleviates Chronic Intermittent Hypoxia-Induced Myocardial Inflammation and Fibrosis via the
Lijun Ou1, Chenyi Liu2, Weicheng Zhao1
1Department of Cardiovascular Disease, The Fourth Clinical College of Guangzhou University of Traditional Chinese Medicine/Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, China.
Insights
Buyang Huanwu decoction (BYHW) protects against chronic intermittent hypoxia (CIH)-induced heart injury in rats by inhibiting the NF-κB/LOX pathway. This traditional Chinese medicine improves cardiac function and reduces inflammation and fibrosis.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Traditional Chinese Medicine
Background:
- Chronic intermittent hypoxia (CIH) is a significant risk factor for myocardial injury.
- Understanding the molecular mechanisms underlying CIH-induced cardiac dysfunction is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the cardioprotective effects of Buyang Huanwu decoction (BYHW) against CIH-induced myocardial injury in a rat model.
- To elucidate the potential regulatory mechanism involving the NF-κB/LOX signaling pathway.
Main Methods:
- Adult Sprague-Dawley rats were subjected to CIH for 5 weeks and treated with BYHW, NF-κB inhibitor (PDTC), or NF-κB agonist (LPS).
- Cardiac function was assessed using echocardiography, and myocardial tissues were analyzed for inflammation and fibrosis.
- Protein and mRNA expression of NF-κB, LOX, Collagen I, and Collagen III were quantified via Western blot and qPCR.
Main Results:
- BYHW treatment significantly improved cardiac function (LVEF, LVFS) and reduced ventricular dilation (LVDd, LVDs) in CIH-induced rats.
- BYHW administration decreased myocardial inflammation, structural disruption, and fibrosis (CVF).
- Molecular analysis showed BYHW significantly reduced NF-κB, LOX, Collagen I, and Collagen III expression, an effect potentiated by PDTC and attenuated by LPS.
Conclusions:
- BYHW demonstrates significant cardioprotective effects against CIH-induced myocardial injury in rats.
- The therapeutic mechanism of BYHW involves the inhibition of the NF-κB/LOX signaling pathway.
- This study provides experimental evidence supporting the use of BYHW for managing CIH-related cardiac complications.
Objective:
To investigate the protective effects of Buyang Huanwu decoction (BYHW) on myocardial injury induced by chronic intermittent hypoxia (CIH) in rats and to analyze its potential regulatory mechanism through the NF-κB/LOX signaling pathway.
Methods:
Then, 36 adult male Sprague-Dawley (SD) rats (weighing 200-250 g) were randomly divided into six groups (n = 6): normal control (NC), CIH model, BYHW, BYHW + lipopolysaccharide (LPS), BYHW + pyrrolidinedithiocarbamate (PDTC), and LPS. Except for the NC group, all groups underwent 5 weeks of intermittent hypoxia (8 h/day) alongside their respective drug treatments. Postintervention, systolic blood pressure and heart rate were recorded. Cardiac function was evaluated by echocardiography to measure left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and left ventricular internal dimension at end-diastole (LVDd) and left ventricular internal dimension at end-systole (LVDs). Myocardial sections were analyzed by HE and Sirius Red staining for quantitative assessment of inflammatory cell infiltration and collagen volume fraction (CVF). The protein and mRNA expression levels of NF-κB, LOX, Collagen I, and Collagen III in cardiac tissue were analyzed by Western blot and qPCR.
Results:
Compared with the NC group, rats exposed to CIH or LPS showed elevated blood pressure and an increased heart rate, along with impaired cardiac function, as evidenced by reduced LVEF (p < 0.05) and LVFS (p < 0.05), along with increased LVDd (p < 0.05) and LVDs (p < 0.05). BYHW treatment significantly ameliorated the CIH-induced cardiac dysfunction and ventricular dilation (p < 0.05), and these improvements were further enhanced by cotreatment with BYHW and the NF-κB inhibitor PDTC (p < 0.05). Conversely, cotreatment with BYHW and the NF-κB agonist LPS attenuated the cardioprotective effects of BYHW (p < 0.05). Histologically, BYHW significantly reduced CIH-induced myocardial structural disruption, inflammatory cell infiltration, and fibrosis (CVF) (p < 0.05), effects that were potentiated by cotreatment with BYHW and PDTC, and counteracted by cotreatment with BYHW and LPS. At the molecular level, Western blot and qPCR analyses revealed that BYHW significantly reduced both the protein and mRNA levels of NF-κB, LOX, Collagen I, and Collagen III (p < 0.05) compared with the NC group. This suppression was further enhanced by cotreatment with BYHW and PDTC and attenuated by cotreatment with BYHW and LPS.
Conclusion:
BYHW improves cardiac function and reduces myocardial inflammation and fibrosis in SD rats with CIH. This effect may be related to the inhibition of the NF-κB/LOX signaling pathway. Cotreatment with BYHW and PDTC enhances this therapeutic effect, while cotreatment with BYHW and LPS attenuates this effect. This study provides preliminary experimental evidence for the cardioprotective effects of BYHW.
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