Retracted: Soluble α-Klotho treatment protects adenine-induced uremia rats from sciatic nerve damage

Neurologic involvement is the most threatening complication of uremic syndrome. Currently, the main treatment of complicated neuropsychic symptom in end-stage uremia is depended on the advent of dialysis and transplant programs, which may associated with many other complications. Effective therapy for this serious and debilitating condition is needed. This study was aimed to elucidate the roles of exogenous α-Klotho (α-KL) on the recovery of injured sciatic nerve induced by uremia. Hematoxylineosin staining was carried out to observe histopathologic changes between the groups. Neurocytes activity was assessed by measuring ATPase, Na+, K+-ATPase, Succinate Dehydrogenase (SDH) activity levels, and NADH as well as NADPH concentrations. NF-kBp65 was assessed to indicate inflammatory. Caspase-3 level was evaluated to indicate the apoptotic pathway. We found that in a damaged nerve induced by uremia, obvious decreased ATPase and Na+, K+-ATPase were observed demonstrating the dysfunction of nerve system conduction, and significant decreased SDH activity, while increased NADH and NADPH levels were observed demonstrating the mitochondrial ROS generation that directly associated with oxidative stress injury and apoptosis, moreover the activation of NF-KBp65 and Caspase-3 singling pathways were observed demonstrating that inflammatory and apoptosis were involved after sciatic nerve being injured. α-KL was effective in the recovery of nerve system conduction, played anti-oxidative stress, anti-inflammatory and anti-apoptosis roles in damaged sciatic nerve, besides promoted the regeneration of peripheral nerve at histopathologic levels. We therefore concluded that α-KL may serve as a potential therapeutic agent for uremia-induced sciatic nerve injury.