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目的:探讨模拟慢性前列腺炎/慢性盆腔疼痛综合征(CP/CPPS)动物模型疼痛产生的分子机制。方法:取SD大鼠36只,随机分为实验组和对照组,每组18只。实验组向前列腺双腹侧叶注射50μl 3%无菌λ-角叉菜胶制作大鼠无菌性前列腺炎症性疼痛模型,对照组注射等量无菌生理盐水。两组分别于造模后1周、2周和4周3个时间节点,每个节点6只大鼠,解剖获取大鼠前列腺组织、L6~S1段背根神经节(DRG)及脊髓,采用免疫组化联合Western印迹法检测神经生长因子(NGF)、瞬时受体电位通道蛋白A1(TRPA1)及降钙素基因相关肽(CGRP)在不同组织内的表达情况。结果:慢性前列腺炎症性疼痛大鼠前列腺组织中NGF、CGRP、TRPA1蛋白的表达均高于对照组(P<0.05),且随造模时间的延长各蛋白表达逐渐减弱,组间比较差异有统计学意义(P<0.05)。在大鼠L6~S1段DRG及脊髓内,造模后1周,实验组NGF、CGRP及TRPA1表达与对照组比较差异无统计学意义(P>0.05),造模后2周及4周,各蛋白表达呈持续高水平状态,与造模后1周大鼠比较差异无统计意义(P>0.05),但各实验组大鼠与对照组蛋白表达比较差异均有统计学意义(P<0.05),两时间点上两组蛋白表达比较差异无统计学意义(P>0.05)。结论:前列腺内注射λ-角叉菜胶方法制作的大鼠前列腺炎症性疼痛模型,可在分子水平模拟CP/CPPS的产生机制;TRPA1在CP/CPPS患者疼痛产生上可能发挥中继通道的作用。
Objective: To investigate the molecular mechanism of pain in simulating chronic prostatitis / chronic pelvic pain syndrome (CP / CPPS) animal model. Methods: Thirty-six SD rats were randomly divided into experimental group and control group, with 18 rats in each group. The experimental group injected 50μl 3% sterile λ-carrageenan into the prostate double-ventral leaves to make aseptic prostatitis rat model of pain, while the control group injected the same amount of sterile saline. The rats were sacrificed at 3 time points of 1 week, 2 weeks and 4 weeks after the model establishment, and 6 rats at each node. The rat prostate tissue, L6-S1 DRG and spinal cord were obtained and dissected. Immunohistochemistry and Western blotting were used to detect the expression of nerve growth factor (NGF), transient receptor potential channel protein A1 (TRPA1) and calcitonin gene related peptide (CGRP) in different tissues. Results: The expression of NGF, CGRP and TRPAl in prostatic tissue of rats with chronic prostatitis pain were significantly higher than that of the control group (P <0.05), and the expression of NGF, Significance (P <0.05). There was no significant difference in the expression of NGF, CGRP and TRPA1 between the experimental group and the control group at 1 week after L6-S1 DRG and spinal cord formation (P> 0.05) There was no significant difference between the two groups (P> 0.05), but there was significant difference in protein expression between the experimental group and the control group (P <0.05) ). There was no significant difference between the two groups in protein expression at two time points (P> 0.05). Conclusions: Prostate inflammatory pain model induced by intra-prostate injection of λ-carrageenin can simulate the mechanism of CP / CPPS at the molecular level. TRPA1 may play a role of relay channel in the pain of CP / CPPS patients .