Current pharmaceutical design · 2026
The Effect of Wei Nai An Capsule on Acute Myocardial Ischemia Complicated with Chronic Atrophic Gastritis via Inflammatory Pathways.
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Dai Wenzhang, Zeng Hekun, Chai Xiaomeng, Cai Kexin, Luo Anqi, Wang Ranjing, Liu Shanshan, Huang Qiuling, Ning Na, Nie Hong
Аннотация
INTRODUCTION: Cardiovascular Diseases (CVDs) and Gastrointestinal Disorders (GIDs) show significant comorbidity. We established a rat model of chronic atrophic gastritis (CAG) complicated by acute myocardial ischemia (AMI) to investigate the protective effects and mechanisms of Wei Nai An Capsule (WNAC) on CAG and AMI.
METHODS: Potential mechanisms were predicted by using network pharmacology and GEO database analysis. To model CAG, we combined intragastric administration of alcohol, sodium deoxycholate, and ammonia. Injections of β-adrenergic agonist isoproterenol modeled the AMI. Histopathological observations were performed, and gastric pH, cardiac marker enzyme levels, cardiac electrical activity, and mRNA expression in the animals were monitored.
RESULTS: Network pharmacology and GEO database analyses suggested that WNAC's positive effect on acute myocardial ischemia complicated by chronic atrophic gastritis is associated with the PI3K-AKT signaling pathway. In the model of acute myocardial ischemia complicated by chronic atrophic gastritis, WNAC significantly decreased the elevated ST-segment on the electrocardiogram, reduced gastric pH, reduced levels of markers of cardiac injury, and reduced the mRNA expression of IκBα, PI3K, NF-κB-p65, and COX2 in cardiac and gastric tissues.
DISCUSSION: This study demonstrated the crucial need to suppress pro-inflammatory pathways in the treatment of the comorbidity between CVDs and GIDs. However, additional experiments could further strengthen the causal inference.
CONCLUSION: This research indicated that WNAC can be successfully implemented to treat the comorbidity of CVDs and GIDs and provides strong evidence for the discovery of new indications of WNAC in clinical practice.
METHODS: Potential mechanisms were predicted by using network pharmacology and GEO database analysis. To model CAG, we combined intragastric administration of alcohol, sodium deoxycholate, and ammonia. Injections of β-adrenergic agonist isoproterenol modeled the AMI. Histopathological observations were performed, and gastric pH, cardiac marker enzyme levels, cardiac electrical activity, and mRNA expression in the animals were monitored.
RESULTS: Network pharmacology and GEO database analyses suggested that WNAC's positive effect on acute myocardial ischemia complicated by chronic atrophic gastritis is associated with the PI3K-AKT signaling pathway. In the model of acute myocardial ischemia complicated by chronic atrophic gastritis, WNAC significantly decreased the elevated ST-segment on the electrocardiogram, reduced gastric pH, reduced levels of markers of cardiac injury, and reduced the mRNA expression of IκBα, PI3K, NF-κB-p65, and COX2 in cardiac and gastric tissues.
DISCUSSION: This study demonstrated the crucial need to suppress pro-inflammatory pathways in the treatment of the comorbidity between CVDs and GIDs. However, additional experiments could further strengthen the causal inference.
CONCLUSION: This research indicated that WNAC can be successfully implemented to treat the comorbidity of CVDs and GIDs and provides strong evidence for the discovery of new indications of WNAC in clinical practice.