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.

Therapeutic potentials of allicin in cardiovascular disease: advances and future directions

“…Recent research indicated that Toll-like receptor 4 (TLR4) and the nuclear factor kappa B (NF-κB) signalling pathway play a role in promoting the activation of cytokines such as TNF-α, IL-6, and IL-1β to exacerbate inflammation, leading to subsequent myocardial tissue damage [ 18 ]. Inhibition or absence of TLR4 or NF-κB, which are critical regulators in pro-inflammatory cascades, had been shown to reduce left ventricular remodelling extent and improve cardiac function [ 19 ]. Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) is an essential protein involved in regulating intracellular calcium transport processes and cardiomyocyte contractile function.…”

“…NF-κB serves as a prototypical pro-inflammatory signalling pathway capable of activating the TGF-β pathway to facilitate myocardial fibrosis [ 69 ]. Kong et al [ 19 ] found that allicin alleviated cardiac dysfunction and decreased myocardial fibrosis in STZ-induced diabetic rats by inhibiting the NF-κB signalling pathway (Table 5 ).…”

“…Kong et al [ 19 ] found that allicin alleviated cardiac dysfunction and decreased myocardial fibrosis in STZ-induced diabetic rats by inhibiting the NF-κB signalling pathway (Table 5 ).…”

The signaling pathways of selected traditional Chinese medicine prescriptions and their metabolites in the treatment of diabetic cardiomyopathy: a review

“…These results suggested that AG has the potential to treat DCM by reducing inflammation and oxidative stress, and its mechanism may be related to NF-κB and NOXs/Nrf2 signaling pathways. Artemisinin and allicin (AA) have anticancer, antioxidant, and anti-inflammatory biological activities ( Zhou et al, 2022 ; Jin et al, 2023 ) and have been proved to be used in clinical anti-myocardial fibrosis ( Kong et al, 2023a ). Kong et al (2023a) found that the cardiac function of STZ-induced diabetic rats was damaged, and AA could improve these damages.…”

“…Artemisinin and allicin (AA) have anticancer, antioxidant, and anti-inflammatory biological activities ( Zhou et al, 2022 ; Jin et al, 2023 ) and have been proved to be used in clinical anti-myocardial fibrosis ( Kong et al, 2023a ). Kong et al (2023a) found that the cardiac function of STZ-induced diabetic rats was damaged, and AA could improve these damages. In addition, the myocardial cells of diabetic rats showed pathological changes, such as increased collagen fibers, a large number of fibrous scars, and increased myocardial cells, and these changes were significantly reduced after AA intervention.…”