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机构地区:[1]河南黄淮学院生物工程系,河南驻马店463000 [2]河南黄淮学院护理学系,河南驻马店463000 [3]驻马店市中心医院泌尿外科,河南驻马店463000
出 处:《中国生化药物杂志》2015年第2期31-34,共4页Chinese Journal of Biochemical Pharmaceutics
基 金:黄淮学院青年骨干教师资助计划;河南省教育厅科技攻关项目(14B180006)
摘 要:目的分析趋化因子CXCL1及受体CXCR2在小鼠骨癌痛模型中的作用,并探讨二磷酸盐对小鼠骨癌痛模型的干预机制。方法 60只小鼠随机分为3组:对照组、模型组和治疗组。股骨远端骨髓腔注射NCTC2742细胞复制小鼠股骨痛模型,治疗组给予二磷酸盐治疗,对照组和模型组给予等量生理盐水。Real-time PCR分析各组中趋化因子CXCL1和CXCR2mRNA的表达,Western blot检测CXCL1、CXCR2蛋白及肿瘤坏死因子TNF-α以及细胞凋亡蛋白Bax/Bcl2以及Caspase-3的表达。结果模型组小鼠的机械缩爪阈值较对照组有显著的增高(P<0.05,P<0.01),而药物治疗组对模型组小鼠的升高的阈值有显著的改善作用(P<0.01);与对照组比较,骨癌痛模型小鼠趋化因子CXCL1及受体CXCR2表达明显增强(P<0.01),二磷酸盐可以显著抑制CXCL1及CXCR2的表达(P<0.01);与对照组比较,骨癌痛模型小鼠肿瘤坏死因子TNF-α、促细胞凋亡蛋白Bax及Caspase-3的表达明显增高,凋亡蛋白Bcl2的表达明显降低(P<0.01),而二磷酸盐可以显著改善上述指标表达(P<0.01)。结论二磷酸盐通过下调骨癌痛模型小鼠趋化因子CXCL1及受体CXCR2表达、促进细胞凋亡发挥治疗骨癌痛模型小鼠的作用。Objective To explore the involvement of CXCL1 and CXCR2 in the pathogenesis of bone cancer pain and the interventions of diphophated. Methods 60 mice were divided into 3 groups randomly: control, model and diphosphated group. The bone cancer pain mice were duplicated by injection of NCTC742 cell while control mice were received same dose of NS. Diphosphate group mice were received diphosphate while control group were received same dose of NS. The expressions of CXCL1, CXCR2, TNF-α and apoptosis proteins were detected by Real-time PCR and Western blot. Results The cancer pain threshold in bone pain model were higher than that of control group ( P 〈 0. 05, P 〈 0. 01 ), while cancer pain threshold in diphosphated group was improved( P 〈 0. 01 ). Compared with control group, the expression of chemotactic factor CXCL1 and its receptor of CXCR2 in model group were up-regulated( P 〈 0. 01 ), while the expression of those parameters were improved( P 〈 0. 01 ). The expression of TNF-α, Bax as well as Caspase-3 were up-regulated and Bcl2 was down-regulated in model group (P 〈 0. 01 ), while diphosphate normalized those parameters with a statistical difference(P 〈0. 01 ). Conclusion Diphosphate alleviates the bone cancer pain by inhibiting the enhanced CXCL1 and its receptor CXCR2 as well as promoting apoptosis.
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