摘要
目的探讨趋化因子Fractalkine在骨癌痛中的作用及其脊髓部位的作用机制。方法采用Walker 256肿瘤细胞,注射在胫骨内建立骨癌痛模型。雌性SD大鼠40只,随机分为5组(n=8),Ⅰ组为Hank’s液对照组,Ⅱ组为骨癌痛组,Ⅲ组为对照组+CX3CR1中和抗体,Ⅳ组为骨癌痛组+IgG;Ⅴ组为骨癌痛组+CX3CR1中和抗体。术后第10～12天,鞘内分别注射CX3CR1中和抗体或IgG,每天1次,剂量10μg/10μl。分别于术前及术后隔日开始测定大鼠机械性痛阈值。术后第12天鞘内注射抗体后6 h处死大鼠,测定脊髓小胶质细胞标志物(OX-42)的表达水平。结果术后第10～12天,与Ⅰ组比较,Ⅱ组、Ⅳ组机械性痛阈值显著下降,脊髓OX-42染色阳性细胞数(Num)及积分吸光度(IA)显著增加,差异均有高度统计学意义(均P<0.01),Ⅲ组上述指标的差异无统计学意义(P>0.05);与Ⅱ组、Ⅳ组比较,Ⅴ组机械性痛阈值显著增高,脊髓OX-42染色Num及IA显著减少,差异均有高度统计学意义(均P<0.01)。结论Fractalkine通过激活脊髓小胶质细胞参与了骨癌痛的形成。
Objective To investigate the role of Fractalkine in pain facilitation and spinal mecha-nisms in the rat model of bone cancer pain.Methods The bone cancer pain model was developed by inoculated Walker 256 mammary gland carcinoma cells into the tibia medullary cavity.Fouty SD female rats were divided into 5 groups（n=8 each） randomly ： groupⅠ： sham operation;groupⅡ：model group;group Ⅲ： control group＋anti-CX3CR intrathecal（IT）;group Ⅳ： model group＋ normal IgG IT,groupⅤ： model group＋anti-CX3CR1 IT.Anti-CX3CR1 or normal IgG was injected IT during 10 to 12th day.Von Frey threshold was measured one day before operation and every 2 days after operation.On the 12th day after operation,rats were sacrificed after IT injection of either anti-CX3CR1 or normal IgG,the lumbar 4-6 spinal cord was removed.The expression of the spinal OX-42（microglial marker） was detected by immunohistochemistry assay.Results From the 10 to 12th day after operation,von Frey threshold in groupsⅡand Ⅳ was significantly lower than that in group I and group Ⅲ（P〈0.01）,groupⅤwas remarkly higher than that in group Ⅳ（P〈0.01）.The spinal OX-42 expression in group Ⅱor Ⅳ was significantly increased compared with that in groupⅠor Ⅲ（P〈0.01）,IT anti-CX3CR1 was significantly suppressed OX-42 expression（P〈0.01）.Conclusion Fractalkine is involved in the bone cancer pain via activation of spinal microglia.
出处
《苏州大学学报（医学版）》
CAS
北大核心
2008年第6期897-899,922,I0009,共5页
Suzhou University Journal of Medical Science
基金
江苏省自然科学研究基金资助项目(2005033)
江苏省卫生厅基金资助项目(K200518)
