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Danshensu attenuates aldosterone-induced cardiomyocytes injury through interfering p53 pathway
Xiaohong Yang1, Rui Yang1, Xianli Li1
1Department of Cardiovascular, Anyang District Hospital, Anyang, Henan 455000, P.R. China.
Insights
Danshensu (DSS) protects heart cells from aldosterone (ALD)-induced injury by reducing apoptosis. DSS interferes with the p53 signaling pathway, offering potential therapeutic benefits for heart failure patients.
Area of Science:
- Cardiovascular Disease Research
- Cellular Biology
- Pharmacology
Background:
- Heart failure is a common cardiovascular disease often resulting from cardiomyocyte loss.
- Excessive aldosterone (ALD) contributes to heart failure by inducing cardiomyocyte hypertrophy and apoptosis.
- Aldosterone directly targets the heart, exacerbating cardiac dysfunction.
Purpose of the Study:
- To investigate the protective effects of danshensu (DSS) against aldosterone-induced injury in cardiomyocytes.
- To elucidate the molecular mechanisms underlying DSS's cardioprotective action.
Main Methods:
- Primary cardiomyocyte cultures were exposed to aldosterone.
- Cell viability and lactate dehydrogenase leakage were measured.
- Apoptosis rates, BAX, Bcl-2, and caspase-3 expression were analyzed.
- The role of the p53 signaling pathway was investigated.
Main Results:
- DSS significantly increased cell viability and reduced lactate dehydrogenase leakage in ALD-exposed cardiomyocytes.
- DSS treatment decreased the apoptotic rate in ALD-stimulated cells.
- DSS modulated the expression of apoptosis-related proteins (BAX, Bcl-2, caspase-3) via the p53 pathway.
Conclusions:
- Danshensu (DSS) demonstrates a protective effect against aldosterone-induced cardiomyocyte injury.
- DSS exerts its beneficial effects by interfering with the p53 signaling pathway.
- These findings suggest DSS as a potential therapeutic agent for managing aldosterone-related heart conditions.
Abstract:
Heart failure, characterized by impaired systolic and/or diastolic function, is a common cardiovascular disease. The loss of cardiomyocytes due to various factors, including through necrosis or apoptosis can result in heart failure. Previous studies have indicated that excessive aldosterone (ALD) serves an essential role in the process of heart failure, and the heart is also one of the direct targets of ALD, which can provoke hypertrophy and the apoptosis of cardiomyocytes. The aim of the present study was to investigate the protective effect of danshensu (DSS) on ALD‑induced cardiomyocytes injury. The present results demonstrated that DSS increased cell viability and decreased the leakage of lactate dehydrogenase in cardiomyocytes exposed to ALD. In addition, DSS decreased the apoptotic rate of ALD‑stimulated cells. Further research indicated that DSS‑ and cellular tumor antigen p53 (p53)‑alone or combination treatment was able to decrease the expression levels of apoptosis regulator BAX and caspase‑3, and increase the expression of apoptosis regulator B‑cell lymphoma (Bcl)‑2 in ALD‑stimulated cardiomyocytes. Taken together, the results of the present study suggest that DSS inhibits the harmful effects of ALD on cardiomyocytes via interfering with the p53 signaling pathway. These results provide novel evidence for the potential protective effects of DSS.