利用长春新碱致神经病理性疼痛小鼠模型,以腹腔注射不同剂量虾青素,通过行为学实验测试机械性缩足反射阈值的变化,并以免疫荧光检测星型胶质细胞和小胶质细胞各自的标记蛋白GFAP和Iba1的蛋白表达变化,以ELISA试剂盒检测炎症因子肿瘤坏死因子α(TNF-α)和单核细胞趋化蛋白1(MCP-1)的表达变化,以此探讨虾青素对长春新碱诱导的神经病理性疼痛的影响及其作用机制.结果表明,虾青素呈剂量依赖性地拮抗长春新碱诱导的神经病理性疼痛(chemotherapy-induced neuropathic pain,CNP)(P<0.01),虾青素能够降低CNP小鼠脊髓胶质细胞GFAP和Iba1的蛋白表达水平以及炎症因子TNF-α和MCP-1的表达水平(P<0.05).虾青素能显著拮抗长春新碱诱导的神经病理性疼痛.%To investigate the effectof astaxanthin on vincristine-induced neuropathic pain and to explore its mechanisms. By behavioral test,mechanical withdrawal threshold(MWT)were tested before and after intraperitoneal administration of different concentrations of astaxanthin on vincristine-induced neuropathic pain mice model. Glial activation markers GFAP and Iba1 expression were determined by immunofluorescence. Spinal production of TNF-α and MCP-1 was quantified by ELISA.We found that astaxanthin dose-dependently inhibited vincristine-induced neuropathic pain(P <0.01). Astaxanthin decreased glial activation and production of cytokines such as TNF-α and MCP-1 in CNP mice(P <0.05). With these results we concluded that astaxanthin attenuate vincristine-induced neuropathic pain significantly. The effect might partly attribute to the inhibition of astrocyte and microglia activation and the decrease of inflammatory cytokines expression associated with the maintenance of neuropathic pain.
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