Role of Vitamin D3 and Alginates in Prevention of NSAID-Dependent Cellular Injury

About 30 million people use nonsteroidal anti-inflammatory drugs. Therefore, they have a high risk of developing gastropathic and enteropathic damages. These patients receive anti-acid treatment, but a number of clinical studies provided evidence of the ineffectiveness of proton-pump inhibitors. Vitamin D, on the other hand, appears to have high preventive and therapeutic potential. Recently, it has been introduced a product that, in addition to anti-acid properties of alginates, claims to possess gastroprotective properties deriving from vitamin D3 and from plant extractsThis study was planned to verify the effectiveness of vitamin D3 combined with alginates to prevent the damage induced in cul-tured gastric cells by diclofenac during acidic or hyperacidic exposition measuring cell viability, radical oxygen species production along with apoptotic and survival pathways.Around 30 million people consume nonsteroidal anti-inflammatory drugs (NSAID) globally every day [1] since they are widely pre-scribed because of their efficacy in the management of pain, inflammation, and fever [2]. Generally, the action mechanism of these drugs consists in the inhibition of the biosynthesis of prostaglandins, the inactivation of cyclooxygenase, and an increase in leukotrienes produc-tion [3]. Adverse events associated with NSAID, such as alterations in renal function, effects on blood pressure, hepatic injury, and plate-let inhibition, are a challenge in clinical treatment optimization [4]. However, severe gastrointestinal disorder accompanied by gastric mucosal perforation and bleeding is a major concern as well as the worst outcome of prolonged NSAID-therapy [5]: indeed, they induce gastric mucosal lesions because of their acidic properties [3]. Gastric mucosal erosions, ulceration, bleeding, and perforation, as well as an increased risk of bleeding from pre-existing peptic ulcers are major causes of gastrointestinal iatrogenic diseases [6]. The mechanism behind gastric damage involves a highly acidic gastric environment that favours the migration of nonionized lipophilic NSAID into the Findings show that this combination is more potent to counteract the negative effects of diclofenac and hyperacidic conditions than some other gastroprotective agents on epithelial gastric cells. This was confirmed by the maintenance of p53 expression at physiological level. In addition, when added before diclofenac, it can exert beneficial effects counteracting the negative effect of diclof-enac alone. These data were similar to the sample treated with pantoprazole, supporting the hypothesis that the combination could act as a gastroprotector to prevent cell loss. These results have pointed out the gastroprotective effect of the combination when compared to other commercial natural ex-tracts, this effect is obtained via antioxidant pathway, inhibiting apoptosis, enhancing cell viability and activating survival kinases