Isoliquiritigenin reduces oxidative damage and alleviates mitochondrial impairment by SIRT1 activation in experimental diabetic neuropathy

depicting the therapeutic potential of ILQ in experimental DN. Mitochondrial derangements occurred due to hyperglycaemia-induced inactivation of SIRT1-AMPK-PGC-1α signalling in experimental DN leads to neuronal dysfunction and nerve damage. ILQ exerts neuroprotection through SIRT1 induction and produces the similar protective effects as that observed with calorie restriction such as promotion of mitochondrial biogenesis, autophagy and oxidative stress resistance. (AMPK: AMP activated protein kinase, FOXO3a: Forkhead box O3, PGC-1α: peroxisome proliferator-activated receptor gamma coactivator 1 alpha, ROS: reactive oxygen species.)194