Laminaran Attenuates NaCl-Induced Cytotoxicity via ROS Scavenging and Prevents Alteration of Cellular Elastic Modulus

Salt is essential for the maintenance of cellular homeostasis and transmission of nerve impulses. However, excessive salt intake (especially NaCl) causes hypertension and neoplasms and is associated with neoplasms, including esophageal and gastric cancer. High concentrations of NaCl enhances intracellular reactive oxygen species (ROS) production, especially that of superoxide anions (O₂^-), and induces injury to rat gastric mucosal cells (RGM1). In contrast, cells overexpressing manganese superoxide dismutase exhibit attenuated NaCl-induced cytotoxicity. Therefore, antioxidants can reduce the risk of salt-induced gastric mucosal injury. NaCl also affects the remodeling of the cytoskeleton and lamellipodia, and potentially modulates the cellular elastic modulus. In this study, we aimed to determine the possibility of cellular physiological changes by NaCl treatment and the effect of antioxidant laminaran in attenuating NaCl-derived cytotoxicity. Our in vitro assay revealed that laminaran attenuated NaCl-induced cytotoxicity and reduced intracellular ROS production caused by NaCl exposure. Laminaran upregulated antioxidant enzyme expression, suggesting that the observed reduction in ROS was mediated, at least in part, by the activation of these enzymes. Moreover, apoptosis derived from NaCl was inhibited by laminaran. NaCl also induced changes in lamellipodia formation; however, laminaran suppressed this formation.