Mechanisms of action of ginger in nuclear factor-kappaB signaling pathways in diabetes

Diabetes mellitus is considered a metabolic disorder characterized by high blood sugar. Active disease is associated with low grade chronic inflammation resulting from the enhanced release of inflammatory mediators such as interleukin (IL)-1 β, IL-6, induced nitric oxide synthase, and cyclooxygenase-2 enzymes that lead to insulin resistance and disease progression. Nuclear factor kappa-B (NF-κB) is a key mediator involved in the inflammatory process which plays an important role in the inflammatory pathogenesis of diabetes. Based on recent evidence, ginger—which contains many phytochemicals—is believed to exert anti-inflammatory properties through multiple mechanisms, such as probably inhibiting the activation of NF-κB signaling pathway. It can thus be a target agent in the treatment and control of diabetes. It appears that ginger may be a complementary agent in diabetes treatment by targeting the NF-κB cascade pathway and exerting antioxidant or anti-inflammatory actions. In this context, this review aims to present the recent evidence regarding the mechanisms of action of ginger in NF-κB signaling pathways in diabetes mellitus.