Abstract
Corticosteroids are used in the treatment of many diseases; however, they also induce various side effects. Dexamethasone is one of the most potent corticosteroids, and it has been reported to induce the side effect of impaired salivary gland function. This study aimed to evaluate the effects of dexamethasone on mouse submandibular gland function to gain insight into the mechanism of dexamethasone-induced salivary hypofunction. The muscarinic agonist carbachol (CCh) induced salivary secretion and was not affected by short-term dexamethasone treatment but was decreased following long-term dexamethasone administration. The expression levels of the membrane proteins Na+-K+-2Cl− cotransporter, transmembrane member 16A, and aquaporin 5 were comparable between the control and long-term dexamethasone treatment groups. The CCh-induced increase in calcium concentration was significantly lower in the presence of extracellular Ca2+ in the long-term dexamethasone treatment group compared to that in the control group. Furthermore, CCh-induced salivation in the absence of extracellular Ca2+ and Ca2+ ionophore A23187-induced salivation was comparable between the control and long-term dexamethasone treatment groups. Moreover, salivation induced by the Ca2+-ATPase inhibitor thapsigargin was diminished in the long-term dexamethasone treatment group. In summary, these results demonstrate that short-term dexamethasone treatment did not impair salivary gland function, whereas long-term dexamethasone treatment diminished store-operated Ca2+ entry, resulting in hyposalivation in mouse submandibular glands.
Highlights
Many medical conditions, including asthma, rheumatoid arthritis, and systemic lupus erythematosus, are treated with corticosteroids, but they induce many side effects.[1]
We found that long-term dexamethasone treatment significantly decreased salivation from ex vivo mouse submandibular gland (SMG), as shown in Fig. 2d, whereas short-term dexamethasone treatment did not have an effect on salivation, and we endeavoured to reveal the details of this mechanism
SMG weights were comparable between the control and Dex[6] groups, and we did not find any apparent differences in the HEstained histological images between the groups, suggesting that dexamethasone-induced salivary hypofunction was not due to any morphological effects
Summary
Many medical conditions, including asthma, rheumatoid arthritis, and systemic lupus erythematosus, are treated with corticosteroids, but they induce many side effects.[1] Increased risks of infection, osteoporosis, fracture, gastrointestinal bleeding, and many other pathologies have been reported as common and severe side effects.[2,3] corticosteroid treatment affects systematic metabolism[4] and decreases the body and organ weights of the liver, thymus, and spleen.[5]. Dexamethasone, a potent glucocorticoid, can cause salivary alterations,[6] and glucocorticoids increase the frequency of experiencing oral dryness.[7] In an animal study, dexamethasone-treated rats exhibited significantly reduced salivary secretion.[8,9] dexamethasone reduced salivary gland mass and increased insulin resistance, which may have a negative impact on salivary gland homeostasis.[9] the mechanism underlying these effects at the cellular level is not well-understood
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