Effect of artemisinin combined with allicin on improving cardiac function, fibrosis and NF-κB signaling pathway in rats with diabetic cardiomyopathy.

Abstract

Myocardial fibrosis and inflammation cause cardiac hypertrophy, arrhythmias, and heart failure in diabetics, a leading cause of mortality. Since it's complicated, no drug treats diabetic cardiomyopathy. This research examined the effects of artemisinin and allicin on heart function, myocardial fibrosis, and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway in diabetic cardiomyopathy rats. A total of 50 rats were separated into 5 groups, 10 of which were the control group. 40 rats received 65 μg/g streptozotocin intraperitoneally. 37 of 40 animals fit the investigation. The artemisinin, allicin, and artemisinin/allicin groups each included nine animals. The artemisinin group received 75 mg/kg of artemisinin, the allicin group received 40 mg/kg of allicin, and the combination group received equal dosages of artemisinin and allicin gavage for four weeks. After the intervention, in each group cardiac functions, myocardial fibrosis, and NF-κB signaling pathway protein expression were assessed. All of the examined groups had greater levels of LVEDD, LVESD, LVEF, FS, E/A, and the NF-κB pathway proteins: NF-κB p65 and p-NF-κB p65 than the normal group, except for the combination group. Artemisinin and allicin did not vary statistically. Compared to the model group, the artemisinin, allicin, and combined groups showed various degrees of improvement from the pathological pattern, with more intact muscle fibers, neater arrangement, more normal cell morphology, artemisinin and allicin alleviated cardiac dysfunction and decreased myocardium fibrosis in diabetic cardiomyopathy rats by inactivating the NF-κB signaling cascade.