【摘 要】
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Background: Cancer-induced pain(CIP)is one of the most severe types of chronic pain with which clinical treatment remains challenging and the involved mechanisms are largely unknown.Suppressor of cyto
【机 构】
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Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases,Institute of
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
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Background: Cancer-induced pain(CIP)is one of the most severe types of chronic pain with which clinical treatment remains challenging and the involved mechanisms are largely unknown.Suppressor of cytokine signaling 3(SOCS3)is an important intracellular protein and provides a classical negative feedback loop,thus involving in a wide variety of processes including inflammation and nociception.However,the role of SOCS3 pathway in CIP is poorly understood.The present study was designed to investigate roles of SOCS3 in dorsal root ganglion(DRG)in the development of CIP.Method: CIP was established by injection of Walker 256 mammary gland tumor cells into the rat tibia canal.Whole-cell patch clamp recordings and western blotting were performed.Results: Following the development of bone cancer,SOCS3 expression was significantly downregulated in rat DRGs at L2-5 segments.Overexpression of SOCS3,using lentiviral-mediated production of SOCS3 at spinal cord level,significantly attenuated mechanical allodynia and body-weight bearing difference,but not the thermal hyperalgesia in bone cancer rats.,Overexpression of SOCS3 also reversed the hyperexcitability of DRG neurons innervating the tibia,and dramatically reduced abnormal expression of toll-like receptors 4 in the DRGs.Conclusions: These results suggest that SOCS3 might be an important molecular involved in the development of the complicated cancer pain and that overexpression of SOCS3 might represent a potential strategy for treatment for mechanical allodynia associated with bone cancer.
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