ArticleCurrent pharmaceutical biotechnology2026
Fufanglongxujie Capsules Protect against Aspirin-induced Gastric Mucosal Lesions in Rats with Myocardial Ischemia-reperfusion Injury.
Article in Current pharmaceutical biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAspirin is frequently employed for the prevention of cardiovascular events, but its clinical utility is hindered by the risk of severe gastrointestinal injury when taken orally. Fufanglongxuejie capsules (FFLXJ), a Chinese patent medicine known for promoting wound healing and alleviating congestion and pain, may offer a promising solution to this clinical challenge.
methodsUsing network pharmacology, candidate targets of FFLXJ, gastrointestinal disorders, intersection targets, and associated signaling pathways were examined. Prior to the creation of myocardial ischemia-reperfusion (MI/R) models, male Sprague-Dawley (SD) rats were orally administered FFLXJ and/or aspirin for a consecutive month. Subsequently, serum motilin (MTL), gastrin (GAS), HE staining, transmission electron microscopy analysis, and western blot analysis were performed on the blood samples or gastric tissues. Molecular docking analysis on core targets and relative compounds was conducted using Discovery Studio software. The expressions of core targets were verified by Western blot.
resultsCompared with aspirin-treated MI/R rats, FFLXJ restored downregulated serum MTL and GAS levels and lessened aspirin-induced gastrointestinal lesions. Network pharmacology research revealed that the top 4 core targets were TNF, IL-10, PTGS2, and VEGFA. In MI/R rats, aspirin treatment markedly increased the level of stomach IL-10, while FFLXJ administration decreased the expression of PTGS2 and IL-10 compared with aspirin-treated group.
conclusionOral aspirin harmed the gastrointestinal mucosa in MI/R rats; however, FFLXJ was able to mitigate the damage. The protective property of FFLXJ was related to the regulation of inflammation.
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