Rebamipide suppresses 5-fluorouracil-induced cell death via the activation of Akt/mTOR pathway and regulates the expression of Bcl-2 family proteins.

摘要: Abstract Oral mucositis is a common adverse effect of chemotherapy that limits the required dose chemotherapeutic agents. Numerous attempts to mitigate chemotherapy-induced oral have failed identify an appropriate treatment. Recently, it has been indicated rebamipide prevents chemoradiotherapy-induced in patients. However, details underlying mechanism involved cytoprotective remain obscure. In present study, we investigated behind mucosa using primary normal human keratinocytes (NHOK cells). We found prevented 5-fluorouracil (5-FU)-induced cell death NHOK cells. addition, increased levels phosphorylated Akt and mTOR, enhanced Bcl-2 Bcl-xL expressions, suppressed expression Bax Bim. This contrast 5-FU-induced suppression mTOR activation, These findings suggest can potentially be used for protection from mucositis. first study elucidates specific molecular pathway rebamipide.