Artemisinin combined with allicin on improving cardiac function, fibrosis, and NF-κB signaling pathway in rats with diabetic cardiomyopathy

Abstract

Background This study aimed to see how artemisinin & allicin affected heart function, myocardial fibrosis, and regulating the nuclear factor-B (NF-B) signaling pathways in the myocardial tissue of diabetic cardiomyopathy rats. Methods 50 rats were selected, 10 of which were kept normally without any intervention as the rest 40 were in the normal group injected intraperitoneally 65 µg/g streptozotocin at one time to construct diabetic cardiomyopathy model.37 rats meeting the criteria for successful model establishment were randomly divided into ten rodents in the model category, 9 rats each in the Artemisinin, Allicin, & Combination groups. For four weeks, the Artemisinin group received 75 mg/kg of artemisinin, the Allicin group received 40 mg/kg of allicin, & the combination group received the same doses of artemisinin & allicin gavage as the Artemisinin & Allicin groups. We investigated the cardiac function, myocardial fibrosis, and the aberrant expression of protein levels in NF-κB signaling pathways in each group after the end of the intervention. Results The model group, Artemisinin group, Allicin group, and combination group showed significantly greater cardiac function indexes, including LVEDD, LVESD, LVEF, FS, and E/A with higher expression of NF-B signaling pathway proteins NF-B-p65 and p-NF-B-p65 than the normal group (P < 0.05). LVEDD, LVESD, LVEF, FS, E/A, and NF-B signaling pathway protein NF-B-p65, and p-NF-B-p65 were significantly decreased in the Artemisinin, Allicin, and combination groups when compared with the modeled group (P < 0.05). The combined group had significantly lower expression of LVEDD, LVESD, LVEF, FS, E/A, NF-B signaling pathway protein NF-B-p65, and p-NF-B-p65 than the Artemisinin and Allicin groups (P < 0.05). For comparing the cardiac function indicators LVEDD, LVESD, LVEF, FS, E/A, NF-B signaling pathway protein NF-B-p65, & p-NF-B-p65 expressions, there was no statistical difference here between Artemisinin & Allicin groups (P > 0.05). After observing the myocardial fibrosis in each group, we found the collagen fibers-associated disorder arrangement of the proliferative network in the modeled group, formation of the fibrous scar with large volume, cardiac hypertrophy, inconsistent coloration, nucleus consolidation, disintegration, and even removal. When compared to the model group, the Artemisinin group, Allicin group, & combined group all demonstrated various degrees of improvement in the problematic structure with more intact muscle fibers, neater arrangement, more normal cell morphology, and more homogeneous staining, with the most significant improvement in the combined group. Conclusion Compared with artemisinin and allicin alone, artemisinin combined with allicin improved cardiac dysfunction and reduced myocardial fibrosis in rats with diabetic cardiomyopathy, and both may act via promoting the inactivation of the NF-κB signaling cascade.