Effects of "Astragalus-Danshen-Sanqi" horn medicine on oxidative stress in rats with heart failure based on network pharmacology and experimental validation

AimTo investigate the effects of Astragalus-Danshen-Sanqi horn medicine on oxidative stress in rats with heart failure model based on network pharmacology and experimental validation.MethodsThe drug active components, core targets and signaling pathways of Astragalus-Danshen-Sanqi horn medicine against oxidative stress in heart failure were screened by network pharmacology, and the core targets were molecularly docked with the drug active components. Forty SD rats were randomly divided into four groups, the control group, model group, horn medicine group and western medicine group, and the corresponding drug interventions were given according to the subgroups. The changes in the level of cardiac function indexes in each group were compared using cardiac ultrasound, the pathological changes in cardiac tissues in each group were evaluated using HE staining, and the fibrosis of cardiomyocytes in each group was assessed using Masson staining; the changes in the ultrastructure of mitochondria of cardiomyocytes in each group were observed using transmission electron microscopy; and the changes in the level of oxidative stress indexes in the cardiac tissues of rats in each group were compared.ResultsThe key pharmacological components screened were quercetin, kaempferol, and lignocerotoxin, and the core targets of action were TNF, IL6, IL1B, TP53, AKT, and CASP3. Animal experiments showed that the cardiac function of rats was significantly improved when compared with that of the model group, and the results of HE and Masson staining showed that the structural damage of myocardial tissues was attenuated, the cardiomyocytes were less fibrous. Electron microscopy revealed reduced mitochondrial structure damage, while ROS levels in myocardial tissue were reduced, and CAT and T-AOC levels increased(P ConclusionHorn medicine is able to exert a protective effect against heart failure by reducing oxidative stress, mitigating mitochondrial structural and functional damage, and promoting the restoration of cardiac systolicdiastolic functions.