Xiangdi Yu1, Chun Chen, Qibin Ke, Heqing Tang, Jun Hou, Wei Fang. 1. Department of Anesthesiology, The First College of Clinical Medical Science, China Three Gorges University, Yichang Central People's Hospital, Yichang, China.
Abstract
BACKGROUND: Neuropathic pain is a well-known type of chronic pain caused by damage to the nervous system. Until recently, researchers have found that increased generation of reactive oxygen species (ROS) contributes to the development of exaggerated pain hypersensitivity during neuropathic pain. METHODS: In this study, we investigated the antinociceptive efficacy of Ginkgo biloba extract (EGb761) in chronic constriction injury (CCI) model of neuropathic pain of rats. To explore the underlying mechanisms, the effects of EGb761 on the excitability of dorsal root ganglion (DRG) neurons and activation of JNK in DRG were explored. RESULTS: We showed that systemic administration of EGb761 inhibited the behavioral responses of neuropathic pain and found that EGb761 treatment could inhibit the H2O2-induced depolarization in the acutely dissociated DRG neurons. In addition, we found that EGb761 treatment could inhibit the expression of p-JNK in DRG. CONCLUSION: Taken together, our results suggest that administration of EGb761 can ameliorate neuropathic pain, and further indicate that JNK, which is activated by both exogenous and endogenous ROS, might be the mechanism underlying the effects of EGb761 on CCI neuropathic pain.
BACKGROUND:Neuropathic pain is a well-known type of chronic pain caused by damage to the nervous system. Until recently, researchers have found that increased generation of reactive oxygen species (ROS) contributes to the development of exaggerated painhypersensitivity during neuropathic pain. METHODS: In this study, we investigated the antinociceptive efficacy of Ginkgo biloba extract (EGb761) in chronic constriction injury (CCI) model of neuropathic pain of rats. To explore the underlying mechanisms, the effects of EGb761 on the excitability of dorsal root ganglion (DRG) neurons and activation of JNK in DRG were explored. RESULTS: We showed that systemic administration of EGb761 inhibited the behavioral responses of neuropathic pain and found that EGb761 treatment could inhibit the H2O2-induced depolarization in the acutely dissociated DRG neurons. In addition, we found that EGb761 treatment could inhibit the expression of p-JNK in DRG. CONCLUSION: Taken together, our results suggest that administration of EGb761 can ameliorate neuropathic pain, and further indicate that JNK, which is activated by both exogenous and endogenous ROS, might be the mechanism underlying the effects of EGb761 on CCI neuropathic pain.