Abstract:Clinical use of non‐steroidal anti‐inflammatory drugs (NSAIDs) is well known to cause gastrointestinal ulcer formation via several mechanisms that include inhibiting epithelial cell migration and mucosal restitution. The drug‐affected signaling pathways that contribute to the toxic side‐effects of NSAIDs are poorly understood. Previous studies have shown that NSAIDs inhibit cell migration in vitro by depolarizing membrane potential and suppressing expression of voltage‐gated potassium channel subunits. Kv1.3, … Show more
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