摘要
目的通过观察香连片对DKK-1 m RNA、β-catenin和PCNA蛋白表达的影响,初步明确香连片预防小鼠溃疡性结肠炎癌变的作用机制。方法 48只BALB/C小鼠随机分为空白组、模型组、香连片用药组和柳氮磺胺嘧啶组,采用DMH/DSS复合法诱导小鼠溃疡性结肠炎癌变模型,造模时间为18周,用药时间为11周。Real-time PCR检测DKK-1基因的表达,SABC免疫组织化学法检测β-catenin和PCNA蛋白的表达。结果 Real-time PCR检测结果表明香连片可以上调DKK-1 m RNA的表达,与模型组比较,差异有统计学意义(P<0.05);免疫组织化学结果表明香连片可以下调β-catenin和PCNA蛋白的表达,与模型组比较,差异具有统计学意义(P<0.05)。结论香连片预防小鼠溃疡性结肠炎癌变的作用机制与上调DKK-1的表达,阻抑Wnt/β-catenin信号通路有一定的关系。
Objective To discuss the mechanism of Xianglian tablets inhibiting the ulcerative colitis carcinogenesis in mice by investigating the expression of DKK-lmRNA,β-catenin and PCNA protein.Methods Sixty BALB/C mice were randomly divided into four groups,blank group,model group,Xiang lian tablet group,and salazosulfadimidine group.The rat model of carcinogenesis was induced by intraperitoneal injection of DMH and oral administration of DSS,with 18 weeks of modeling time and 10 weeks of medication.DKK-1mRNA expression was detected by RT-PCR and the expression of β-catenin and PCNA protein were measured by immunohistochemistry.Results RT-PCR test showed Xianglian tablets increased DKK-1mRNA expression,compared with the model group(P<0.05).Immuneohistochemistry showed Xianglian tablets decreased the expressions of β-catenin and PCNA protein,compared with the model group(P<0.05).Conclusion The mechanism of Xianglian tablets inhibiting the mice ulcerative colitis canceration is associated with upregulating DKK-1mRNA expression and preventing Wnt/β-catenin signal transduction.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2014年第12期1276-1278,共3页
Cancer Research on Prevention and Treatment
基金
上海市教委项目(2011JW07)