Sodium Alginate Attenuates H2O2-Induced Myocardial DNA Damage via VSNL1 Regulating the CNP/NPR-B Signaling Pathway

Myocardial DNA damage plays a critical role in the pathogenesis of cardiovascular diseases, frequently leading to adverse outcomes such as myocardial infarction and heart failure. This study elucidated the protective effects of sodium alginate (SA) against myocardial DNA damage and explored the underlying molecular mechanisms involved. Hydrogen peroxide (H₂O₂) -stimulated AC16 cells were employed as an in vitro model to induce myocardial DNA damage, and CCK-8 assays established that SA exhibited no cytotoxicity at concentrations up to 800 µM. The protective effects of SA on myocardial DNA damage were shown to be mediated by VSNL1 using immunofluorescence, western blotting and qPCR analyses. To further substantiate this mechanism, lentiviral transduction was utilized to achieve VSNL1 overexpression, whereas targeted siRNA silencing was employed for VSNL1 knockdown. Following VSNL1 overexpression, a reduction in γ-H2AX protein expression was observed, accompanied by increased levels of CNP and NPR-B proteins on the cell membrane, as well as a decrease in intracellular calcium ion concentrations. Conversely, knockdown of VSNL1 reduced the protective effects of SA, highlighting its critical role in the mediation of cardioprotective mechanisms. Taken together, these findings suggest that SA exerts a potential protective effect against myocardial DNA damage through upregulating VSNL1, activating the CNP/NPR-B signaling pathway, and decreasing intracellular calcium ion accumulation. These results underscore that SA is a promising therapeutic candidate for the attenuation of myocardial injury.