• Behavioural pharmacology · Aug 2015

    Antinociceptive activity of astragaloside IV in the animal model of chronic constriction injury.

    • Guo-Bing Shi, Rong Fan, Wei Zhang, Chen Yang, Qi Wang, Juan Song, Yue Gao, Ming-Xiao Hou, Yu-Feng Chen, Tong-Chao Wang, and Guo-Jun Cai.
    • aDepartments of Orthopaedic Surgery bPharmacy cUltrasonography, General Hospital of Shen-yang Military Area Command, Shenyang dDepartment of Orthopaedic Surgery, Changzheng Hospital eDepartment of Pharmacology, The Second Military Medical University, Shanghai, People's Republic of China.
    • Behav Pharmacol. 2015 Aug 1; 26 (5): 436-46.

    AbstractTo investigate the applicability of astragaloside IV (AG) for the treatment of refractory neuropathic pain, we systemically evaluated the antinociceptive activity of AG in the animal model of chronic constriction injury. We studied behaviors, electrophysiology, and biochemistry from day 2 to day 23 after the surgery. We found that when administered intraperitoneally at the dose of 60 mg/kg, AG caused significant inhibition of allodynia and hyperalgesia induced by mechanic and thermal stimuli as well as downregulation of the expressions of a series of proteins involved in mediating neuropathic pain in the dorsal root ganglia, such as P2X purinoceptor 3, glial cell-derived neurotrophic factor, glial cell-derived neurotrophic factor family receptor α1, and transient receptor potential cation channel subtypes A1 and V1. Further investigation showed that AG restored the nerve conduction velocity and the histological structure of the damaged sciatic nerve on day 23 after the surgery. Moreover, results from immunoelectron microscope showed that glial cell-derived neurotrophic factor family receptor α1 induced by AG could form a circular band in the myelin debris between the injured axons and Schwann cells, contributing toward restoration of the damaged nerve. In conclusion, in our animal model, AG effectively inhibited the neuropathic pain induced by chronic constriction injury.

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