Abstract
Background Araloside C (AsC), a natural saponin isolated from Aralia elata, has a wide range of anti-inflammatory properties and has been found in recent years to have heart-protective effects. Present study aimed to determine the effects of AsC on myocardial cell apoptosis through regulating PI3K/AKt. Methods and Results Statistical analyses were performed using GraphPadPrism7.0 software. The differences between two groups and multiple groups were analyzed using t-test and one-way ANOVA, respectively. In vivo results showed that AsC administration could improve cardiac functions and apoptotic rate in HF model through PI3K/AKt signaling pathway, including increasing left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS), and decreasing left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) in detection of myocardial function, inhibiting LDH, CK, CK-MB, CK and HBDH in biochemical index level assessment, inhibiting BNP, ANG II, IL-1b, IL-4, IL-6 and TNF-a in immunological index level. ASC regulates the expression of key apoptotic molecules, including increasing the expression of Bcl-2 and Bax. ASC also regulates phosphorylation of p-PI3K and p-Akt.Conclusion This study suggested for the first time that AsC could partially regulate the PI3K/AKt signaling pathway to prevent myocardial cell apoptosis. This study provided a basis for further research on effective substances in the treatment of HF.
Increased B-type-natriuretic peptide promotes myocardial cell apoptosis via the B-type-natriuretic peptide/long non-coding RNA LSINCT5/caspase-1/interleukin 1β signaling pathway
