Neurotherapeutic Potential of Cervus elaphus Sibericus on Axon Regeneration and Growth Cone Reformation after H2O2-Induced Injury in Rat Primary Cortical Neurons

Abstract

Simple Summary Oxidative stress plays a crucial role in nerve injury-induced changes, including the cellular redox state, greater disease severity, and reduced function. Most studies have demonstrated that the modulation of oxidative damage to neurons leads to improved survival and functional recovery. Deer antlers are considered a potent natural source of antioxidants. Thus, we examined the neurotherapeutic effect of Cervus elaphus sibericus in the axon regeneration and growth cone reformation of cortical neurons. The effect of three doses of C. elaphus sibericus on cortical neurons was determined in a hydrogen peroxide-induced injury model using immunocytochemistry, flow-cytometry, and real-time PCR. We found that C. elaphus sibericus effectively inhibited neuronal death following hydrogen peroxide-induced injury by significantly inhibiting oxidative stress and consequently promoting neuron repair and axon regeneration in cortical neurons. Abstract Cervus elaphus sibericus (CES), commonly known as deer antler, has been used as a medicinal herb because of its various pharmacological activities, including its anti-infective, anti-arthritic, anti-allergic, and anti-oxidative properties. However, the precise mechanisms by which CES functions as a potent anti-oxidative agent remain unknown; particularly, the effects of CES on cortical neurons and its neurobiological mechanism have not been examined. We used primary cortical neurons from the embryonic rat cerebral cortex and hydrogen peroxide to induce oxidative stress and damage in neurons. After post-treatment of CES at three concentrations (10, 50, and 200 µg/mL), the influence of CES on the neurobiological mechanism was assessed by immunocytochemistry, flow cytometry, and real-time PCR. CES effectively prevented neuronal death caused by hydrogen peroxide-induced damage by regulating oxidative signaling. In addition, CES significantly induced the expression of brain-derived neurotrophic factor and neurotrophin nerve growth factor, as well as regeneration-associated genes. We also observed newly processing elongated axons after CES treatment under oxidative conditions. In addition, filopodia tips generally do not form a retraction bulb, called swollen endings. Thus, CES shows therapeutic potential for treating neurological diseases by stimulating neuron repair and regeneration.