LAUSR

Oxidative stress is the core problem in improving secondary spinal cord injury (SCI). To investigate the effect of electro-acupuncture with different frequencies on neuroinflammation, oxidative stress injury, as well as related signaling pathways, male Sprague-Dawley (SD) rats were induced using operation for model SCI and then treated with electrical stimulation at low frequency (2 mA, 0.2 Hz), medium frequency (2 mA, 50 Hz), and high frequency (2 mA, 100 Hz), respectively. Here, we first demonstrated that the JNK/p66 Shc signal pathway promoted ROS generation and inhibited the anti-oxidation effect of FoxO3a to induce oxidative stress damage after SCI and the mechanism of electro-acupuncture in anti-oxidative stress. Electro-acupuncture facilitated functional recovery after SCI and improved the apoptosis of neurons. Furthermore, p38MAPK-mediated microglia activation and inflammatory reaction and JNK/p66 Shc -mediated ROS generation and oxidative stress damage were both attenuated by electro-acupuncture. However, the inhibitory effect of electro-acupuncture on p38MAPK was enslaved to the acupuncture frequency, but the ROS generation and phosphorylation of p66 Shc were effectively inhibited by electro-acupuncture. Therefore, the activation of JNK/p66 Shc promoted the ROS-induced oxidative stress damage after SCI, and inhibiting the phosphorylation of p66 Shc -mediated oxidative stress was the key target of electro-acupuncture to facilitate functional recovery SCI, but not p38MAPK.