Key result
Aconitine promotes cardiomyocyte injury and apoptosis by inhibiting autophagy via ROS-dependent P38/MAPK signaling.
Why the study?
The mechanism of cardiotoxicity induced by aconitine is limited and requires investigation to understand myocardial injury pathways.
p-value: p=<0.01
Aconitine induces cardiotoxicity in vitro by activating the ROS-mediated P38/MAPK/Nrf2 pathway, leading to increased apoptosis and altered autophagy.
Aconitine exposure may warrant cardiotoxicity caution; leaves open in vivo and clinical translation of the ROS-P38/MAPK/Nrf2 pathway.
BACKGROUND: Aconitine has cardiotoxicity, but the mechanism of cardiotoxicity induced by aconitine is limited. The aim of this study was to investigate the mechanism of myocardial injury induced by aconitine. METHODS: Using aconitine, ROS inhibitor N-acetylcysteine(NAC), the autophagy activitor Rapamycin (Rap) or the P38/MAPK pathway activitor Dehydrocorydaline treats H9C2 cells. CCK-8 assay was used to assay cell proliferation activity. Flow Cytometry was used to detect cell apoptosis. Dichloro-dihydrofluorescein diacetate was used to detect ROS levels. The expression of LC3 was detected by Immunofluorescence Staining. Western blotting detected the expression of related proteins. The mRNA levels of inflammatory factors were detected by RT-qPCR. RESULTS: Aconitine inhibits cardiomyocyte proliferation, induces apoptosis and secretion of inflammatory factors. Aconitine activates the P38/MAPK/Nrf2 pathway, induces ROS increase, and promotes autophagy. NAC can inhibit proliferation inhibition, apoptosis, inflammation and P38/MAPK/Nrf2 pathway activation induced by aconitine. Rap and P38 activators can partially recover the effects of NAC on proliferation, apoptosis, inflammation and autophagy of cardiomyocytes. CONCLUSION: Aconitine promotes ROS-activated P38/MAPK/Nrf2 pathway to inhibit autophagy and promote myocardial injury.
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Yang et al. (2024) studied Cardiotoxicity. Aconitine vs. Untreated control was evaluated on Cell viability, apoptosis, and ROS levels (p=<0.01). Aconitine promotes myocardial injury and apoptosis in H9C2 cells by inhibiting autophagy through the ROS-activated P38/MAPK/Nrf2 signaling pathway.
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