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作 者:陆斌[1] 辛欠欠 张军峰[2] 王瑞平[3] 杨亚平[2] 詹瑧[2] LU Bin(Department of oncology,Yangzhong people's hospital,Yangzhong,Jiangsu,212200,China)
机构地区:[1]扬中市人民医院肿瘤内科,江苏扬中212200 [2]南京中医药大学,江苏南京210023 [3]江苏省中医院肿瘤内科,江苏南京210029
出 处:《齐齐哈尔医学院学报》2020年第1期12-16,共5页Journal of Qiqihar Medical University
摘 要:目的探讨胃癌脾胃虚弱证的炎症免疫机制。方法选择2014年4月-2015年12月在江苏省中医院、扬中市人民医院招募病理学诊断明确的原发性胃癌患者160例作为研究对象,分为胃癌脾胃虚弱证组(71例)和胃癌无证组(89例)两组;另选同期正常体检者81名作为对照组。电化学发光免疫检测血清20种炎性因子,进行多因素统计分析。结果与对照组相比,胃癌无证患者血清IL-12/IL-23p40、IL-15、IL-17α、IL-1β、IL-2、IL-8、IL-10、TNF-α显著升高(P<0.05),胃癌脾胃虚弱证患者血清IL-8、IL-10、TNF-α显著升高(P<0.05),但胃癌无证和脾胃虚弱证患者无显著差异(P>0.05)。聚类分析显示,胃癌无证患者IFN-γ和IL-15显著正相关,胃癌脾胃虚弱证患者IL-4和IL-16显著正相关,分别与上皮内1型固有淋巴样细胞和嗜酸性粒细胞活化相关。结论胃癌脾胃虚弱证具有特定的血清炎性因子表达模式,可能与消化道黏膜固有炎症免疫相关。Objective This study aimed to investigate the inflammatory immune mechanism in spleenstomach deficiency syndrome for the patients with gastric cancer.Methods From April 2014 to December 2015 a total of 160 cases of patients with primary gastric cancer that confirmed by pathological diagnosis were recruited from Jiangsu TCM hospital and people’s hospital of Yangzhong city.Seventy-one patients were divided into spleen-stomach deficiency syndrome group and the other 89 patients were in no syndrome group and 81 healthy individuals were recruited as controls.The serum levels of 20 inflammatory cytokines were measured by electrochemiluminescence assay and multivariate statistical analysis was conducted.Results Compared with the healthy controls,the serum levels of 8 inflammatory cytokines(IL-12/IL-23 P40、IL-15,IL-17α,IL-1β,IL-2,IL-8,IL-10,TNF-α)distinctly increased in the GC patients with no syndrome(P<0.05),and the serum levels of 3 inflammatory cytokines(IL-8,IL-10,TNF-α)distinctly increased in the GC patients with spleen-stomach deficiency syndrome(P<0.05).However,no differences were observed between the GC patients with spleen-stomach deficiency and no syndrome.Cluster analysis showed that the IFN-γand IL-15 in the GC patients with no syndrome was relevant to the activation of intraepithelial type 1 innate lymphoid cells,and the IL-4 and IL-16 in the GC patients with spleen-stomach deficiency syndrome was relevant to the activation of eosinophils.Conclusions Spleen-stomach deficiency syndrome presented to have a pathognomonic expression pattern of serum inflammatory cytokines,which potentially involved the mucosal innate inflammatory immunity in the gut.
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