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作 者:高燕 刘芝兰[1] 杨玉霞 白菊芳 冶挺 乌仁娜 GAO Yan;LIU Zhi-lan;YANG Yu-xia;BAIJu-fang;YE Ting;WU Ren-na(Qinghai Provincial People's'Hosbital,Xining,Qinghai 810000,China;不详)
机构地区:[1]青海省人民医院消化内科,青海西宁810000 [2]青海省人民医院控制感染科,青海西宁810000 [3]青海省海西州德令哈市火车站社区卫生服务中心内科,青海海西817099
出 处:《中华医院感染学杂志》2022年第23期3601-3604,共4页Chinese Journal of Nosocomiology
基 金:青海省医药卫生科技项目资助(2019-wjzdx-21)。
摘 要:目的分析胃癌组织中幽门螺杆菌(Hp)感染与胃泌素-17(G-17)、保罗样激酶1(PLK1)表达的相关性。方法选取2018年1月-2021年1月于医院诊治的150例胃癌患者,根据患者是否Hp感染分为感染组和未感染组,比较两组患者G-17、胃蛋白酶原(PG)、炎性因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)、C-反应蛋白(CRP)]、PLK1、转录激活因子3(STAT3)mRNA水平,使用免疫组织化学法检测两组PLK1、STAT3表达情况,并分析胃癌患者G-17和炎性因子、PLK1与STAT3表达和Hp感染的相关性。结果两组胃癌患者的病理分型比较,差异有统计学意义(P<0.05);感染组的G-17、PG-Ⅱ、STAT3和PLK1 mRNA水平,以及CRP、IL-8和TNF-α水平均高于未感染组(P<0.05);胃癌患者G-17与CRP、IL-8和TNF-α水平均呈正相关(P<0.05);胃癌患者PLK1与STAT3表达呈正相关(P<0.05);Hp阳性患者的PLK1、STAT3蛋白阳性率均高于Hp阴性患者(P<0.05)。结论Hp感染的胃癌患者中PLK1、STAT3高表达,同时G-17、PG-Ⅱ及炎性因子水平异常上调,Hp感染和PLK1/STAT3信号通路激活可能参与胃癌的发生。OBJECTIVE To analyze the correlation between Helicobacter pylori(Hp)infection and the expression of gastrin-17(G-17)and Paul-like kinase 1(PLK1)in gastric cancer tissues.METHOD A total of 150 patients with gastric cancer treated in the hospital between Jan 2018 and Jan 2021 were enrolled.According to whether Hp infection occurred,they were divided into the infection group and non-infection group.The levels of G-17,pepsinogen(PG),inflammatory factors[tumor necrosis factor-α(TNF-α),interleukin-8(IL-8),C-reactive protein(CRP)],PLK1 and STAT3 mRNA between the two groups were compared.The expressions of PLK1 and STAT3 in both groups were detected by immunohistochemistry.The correlation between G-17,inflammatory factors,PLK1 and STAT3 and Hp infection was analyzed by spearman method.RESULTS The differences in pathological classifications between the two groups were significant(P<0.05).The levels of G-17,PG-Ⅱ,STAT3,PLK1 mRNA,CRP,IL-8 and TNF-αin the infection group were higher than those in the non-infection group(P<0.05).G-17 was positively correlated with CRP,IL-8 and TNF-αlevels(P<0.05).PLK1 was positively correlated with STAT3 in gastric cancer patients(P<0.05).The positive rates of PLK1 and STAT3 protein in Hp-positive patients were higher than those in Hp-negative patients(P<0.05).CONCLUSION The expression of PLK1 and STAT3 are up-regulated,and levels of G-17,PG-II and inflammatory factors in gastric cancer patients with Hp infection are extraordinary high.Hp infection and activation of PLK1/STAT3 signaling pathways may be involved in the occurrence of gastric cancer.
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