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| CaM/CaMK-Ⅱ信号通路在小鼠炎性痛中的作用 |
| The role of CaM/CaMK-Ⅱ signaling pathways in inflammatory pain in mice |
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| DOI：10.12089/jca.2017.12.1207 |
| 中文关键词: 钙调蛋白/钙调素依赖蛋白激酶Ⅱ 环磷腺苷效应元件结合蛋白 c-fos 炎性痛 |
| 英文关键词: CaM/CaMK-Ⅱ CREB c-fos Inflammation pain |
| 基金项目:内蒙古自治区人民医院博士科研启动资金(BS201511) |
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| 中文摘要: |
目的 探讨钙调蛋白/钙调素依赖蛋白激酶Ⅱ（CaM/CaMK-Ⅱ）信号通路在C57BL6小鼠炎性痛中的作用。
方法 选取体重25～27 g的雄性C57BL6小鼠60只, 随机分为对照组(C组)、完全弗氏佐剂(CFA)组(F组)和KN-93+CFA组(KF组), 每组20只。C组小鼠右侧后爪趾底注射生理盐水50 μl, F组注射50 μl CFA制备炎性痛模型, KF组注射CFA前30 min 鞘内注射DMSO稀释的终浓度为10 mmol/L的KN-93。分别于右侧后爪趾底注射前30 min、注射后1 h和4 h测定小鼠热刺激缩足潜伏期(TWL); 取小鼠脊髓组织, 采用Western blot法检测p-CaMK-Ⅱ、p-CREB、c-fos蛋白含量; RT-PCR法检测CaMK-Ⅱ、CREB、c-fos基因表达。
结果 注射后1 h和4 h, F和KF组TWL明显短于C组,但KF组明显长于F组(P<0.05); F组和KF组脊髓组织p-CaMK-Ⅱ、p-CREB及c-fos蛋白含量和基因表达量均明显高于C组, 但KF组明显低于F组(P<0.05)。
结论 CaM/CaMK-Ⅱ信号通路参与小鼠炎性痛的发生与发展。 |
| 英文摘要: |
Objective To investigate the role of CaM/CaMK-Ⅱ signaling pathways in inflammatory pain in mice.
Methods Sixty male C57BL6 mice, weighing 25-27 g, were randomly divided into 3 groups (n=20): control group (group C), complete freunds adjuvant (CFA) group (group F) and KN-93+CFA group (group KF). Saline 50 μl were injected into the right side of the claw in group C. CFA 50 μl were injected into the right claw foot for the preparation of inflammatory pain models in group F. KN-93 45 nmol was injected i. c. v. 30 min before CFA injection in group KF. The thermal withdrawal latency (TWL) were measured 30 min before injection, 1 h and 4 h after injection. The protein expressions of CaMK-Ⅱ, c-fos and CREB in the spinal cord were measured at above time by Western blot.
Results Compared with group C, TWL were lower in groups F and KF 1 h and 4 h after injection (P<0.05). Compared with groups F, TWL in group KF were higher 1 h and 4 h after injection (P<0.05). Compared with group C, the protein expressions of p-CaMK Ⅱ, p-CREB, c-fos and mRNA expression of CaMK-Ⅱ, CREB, c-fos were higher in group F and KF 1 h and 4 h after injection (P<0.05). Compared with group F, the protein expression of p-CaMK-Ⅱ, p-CREB, c-fos and mRNA expressions of CaMK-Ⅱ, CREB, c-fos in group KF were lower 1 h and 4 h after injection (P<0.05).
Conclusion CaM/CaMK-Ⅱ signaling pathways involved in inflammatory pain in mice. |
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