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南京医科大学学报(自然科学版)                                 第42卷第10期
               ·1364 ·                    Journal of Nanjing Medical University(Natural Sciences)  2022年10月


             ·基础医学·

              大黄素对CFA诱导小鼠炎性痛的治疗作用及机制



              郑 湘 ,吴周全 ,符国伟 ,赵             琳 ,恽惠方    2*
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               南京医科大学附属常州第二人民医院疼痛科,麻醉科,江苏                     常州 213003
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             [摘    要] 目的:研究大黄素(emodin)对弗氏完全佐剂(complete Freund’s adjuvant,CFA)诱发的小鼠炎性疼痛的治疗作用及
              其可能的分子机制。方法:CFA注射于C57BL/6小鼠右后爪足背侧皮下诱导炎性疼痛模型,并用大黄素溶液腹腔注射进行干预。疼
              痛阈值通过 von Frey 试验和热板试验进行评估。RT⁃qPCR 和 ELISA 测定炎症细胞因子肿瘤坏死因子(tumor necrosis factor,
              TNF)⁃α、白细胞介素(interleukin,IL)⁃1β和IL⁃6的表达。Western blot检测背根神经节(dorsal root ganglion,DRG)中瞬时受体电位
              香草酸 1(transient receptor potential vanillic acid 1,TRPV1)和瞬时受体电位香草酸 4(transient receptor potential vanillic acid 4,
              TRPV4)蛋白表达。结果:CFA组小鼠的机械疼痛和热痛阈值显著低于对照组(P < 0.05)。大黄素治疗可显著提高 CFA 诱导
              的炎性疼痛小鼠的机械疼痛和热痛阈值(P < 0.05)。与对照组相比,大黄素干预能够显著降低CFA炎性疼痛小鼠DRG和血
              清中炎症细胞因子TNF⁃α、IL⁃1β、IL⁃6以及DRG中TRPV1和TRPV4的表达水平(P < 0.05)。结论:大黄素可能通过下调DRG
              和血清中炎症细胞因子TNF⁃α、IL⁃1β、IL⁃6以及DRG中疼痛相关离子通道TRPV1和TRPV4的表达来缓解CFA诱导的炎性疼
              痛。
             [关键词] 大黄素;炎性疼痛;弗氏完全佐剂;炎症因子;TRPV1;TRPV4
             [中图分类号] R364.5                    [文献标志码] A                      [文章编号] 1007⁃4368(2022)10⁃1364⁃08
              doi:10.7655/NYDXBNS20221003


              Therapeutic effect and mechanism of emodin on CFA induced inflammatory pain in mice

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              ZHENG Xiang ,WU Zhouquan ,FU Guowei ,ZHAO Lin ,YUN Huifang  2*
              1 Department of Pain,Department of Anesthesiology,Changzhou Second People’s Hospital Affiliated to Nanjing
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              Medical University,Changzhou 213003,China
             [Abstract] Objective:To study the therapeutic effect of emodin on inflammatory pain induced by complete Freund’s adjuvant
             (CFA)in mice and its possible molecular mechanism. Methods:CFA was injected subcutaneously on the dorsal side of the right hind
              paw of C57BL/6 to induce an inflammatory pain model,and emodin solution was injected intraperitoneally for intervention. The pain
              threshold was evaluated by the von Frey test and the hot plate test. qRT⁃PCR and ELISA measure the expression of inflammatory
              cytokines tumor necrosis factor α(TNF⁃α),interleukin⁃1β(IL⁃1β)and interleukin⁃6(IL⁃6). Western blot was used to detect the
              expression of transient receptor potential vanillic acid 1(TRPV1)and transient receptor potential vanillic acid 4(TRPV4)in dorsal
              root ganglion(DRG). Results:The mechanical pain and thermal pain thresholds of mice in the CFA group were significantly lower than
              those of the control group(P < 0.05). Emodin treatment significantly increased mechanical pain and thermal pain threshold in mice
              with induced inflammatory pain(P < 0.05). Compared with the control group,emodin intervention can not only significantly reduce the
              inflammatory cytokines TNF ⁃ α,IL ⁃ 1β and IL ⁃ 6 in DRG and serum of mice with CFA inflammatory pain,but also reduce the
              expression levels of TRPV1 and TRPV4 in DRG(P < 0.05). Conclusion:Emodin relieves CFA ⁃ induced inflammatory pain by
              reducing the content of inflammatory cytokines TNF⁃α,IL⁃1β and IL⁃6 in DRG and serum,and down⁃regulating the expression of pain⁃
              related ion channels TRPV1 and TRPV4 in DRG.
             [Key words] emodin;inflammatory pain;CFA;inflammatory factor;TRPV1;TRPV4
                                                                      [J Nanjing Med Univ,2022,42(10):1364⁃1370,1401]




             [基金项目] 常州市第十五批科技计划(科技支撑-社会发展)项目(CE20155051)
              ∗
              通信作者(Corresponding author),E⁃mail:yhfdoctor@163.com
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