摘要
目的观察坐骨神经分支选择性损伤(SNI)模型大鼠不同时间点术侧腰段L4~L6脊髓背角神经元磷酸化p38丝裂原活化蛋白激酶(p-p38MAPK)和磷酸化活化转录因子2(p-ATF2)的表达情况,探讨脊髓背角p-p38MAPK和p-ATF2在神经病理性痛模型不同阶段中的作用。方法健康雄性SD大鼠36只,完全随机分为空白对照组、假手术组和手术组,各12只。通过结扎腓总神经及切断胫神经,保留腓肠神经的方法建立SNI大鼠模型。观察造模前、造模后3天和14天术侧足跖缩足阈值(PWT);免疫荧光法检测造模后3天和14天术侧腰段脊髓背角p-p38MAPK和p-ATF2阳性细胞表达情况。结果选模后3天和14天,手术组大鼠术侧足跖PWT较假手术组与空白对照组明显降低(P<0.01),假手术组大鼠与空白对照组大鼠比较差异无统计学意义(P>0.05)。造模后3天和14天,手术组大鼠术侧腰段脊髓背角p-p38MAPK和p-ATF2阳性细胞表达率较假手术组和空白对照组均明显升高(P<0.01),假手术组和空白对照组SNI模型大鼠造模后各时间点,术侧腰段脊髓背角p-p38MAPK和p-ATF2阳性细胞表达率差异均无统计学意义(P>0.05)。结论 SNI模型神经病理痛的产生和维持可能与术侧腰段脊髓背角p-p38MAPK和p-ATF2表达上调有关。
Objective To investigate the changes of p-p38MAPK and p-ATF2 expression in ipsilateral L4-L6 spinal cord dorsal horn（SCDH） of ratsat different times of the spared nerve injury（SNI）, and to probe into the effect of central p-p38MAPK and p-ATF2 in neuropathic pain. Methods Thirty-six healthy male SD rats were randomly divided into control group, sham surgery group and surgery group. The spared nerve injury model was established by ligating the common peroneal and the tibial nerves and then cutting off the nerves but keeping the sural nerve intact. Ipsilateral paw withdrawal threshold（PWT） were measured. The levels of p-p38MAPK and p-ATF2 in ipsilateral SCDH were tested by immunofluorescence. Results Rats in surgery group developed spontaneous pain and showed a significant reduction in PWT on D3 and D14（P〈0.01）, while that of sham surgery did not show a significant reduction （P〉0.05）. P-p38MAPK and p-ATF2 expression in ipsilateral L4-L6 SCDH of spared nerve injury rats increased on D3 and D14 after injury（P〈0.01, P〈0.01 ）. There was no difference of p-p38MAPK and p-ATF2 expression in ipsilateral L4-L6 SCDH between control group and sham surgery group （P〉0.05）. Conclusion The induction and maintainence of spared nerve injury-induced neuropathic pain were associated with the activation of p-p38MAPK and p-ATF2 in ipsilateral SCDH.
出处
《浙江中西医结合杂志》
2017年第4期271-274,F0003,共5页
Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
基金
浙江省自然科学基金(No.LY14H270002
No.LY14H270007)
浙江省重点科技创新团队计划资助(No.2013TD15)
