潘崇南 王星钧 金辉

[摘要] 目的 探討基于氨基末端激酶（JNK）/p38通路调控微小RNA-7（miR-7）对幽门螺杆菌（Hp）感染诱导的结直肠癌大鼠的干预作用。 方法 选取60只雄性SD大鼠，15只作为正常组，其余45只建立Hp感染诱导的结直肠癌模型，并随机分为模型组、上调组、下调组各15只。上调组、下调组做miR-7转染。鉴定miR-7转染效率，比较每组检出率，测定Th17/Treg相关因子mRNA表达水平及JNK/p38通路蛋白表达量。 结果 与正常组相比，其他三组miR-7、Foxp3、IL-10表达较低，IL-17A、IL-21、JNK、p38表达较高（P<0.05）;与模型组相比，下调组miR-7、Foxp3、IL-10表达较低，IL-17A、IL-21、JNK、p38表达较高，上调组miR-7、Foxp3、IL-10表达较高，IL-17A、IL-21、JNK、p38表达较低（P<0.05）。 结论 上调miR-7可改善机体的免疫能力，减缓结直肠癌的发生进程，其作用机制可能与JNK/p38通路有关。

[关键词] 结直肠癌;幽门螺杆菌感染;氨基末端激酶;微小RNA-7

[中图分类号] R587.2          [文献标识码] A          [文章编号] 1673-9701（2021）35-0024-03

Intervention of miR-7 on colorectal cancer rats induced by Hp infection based on JNK/p38 pathway analysis

PAN Chongnan1   WANG Xingjun2   JIN Hui3

1.Department of Infectious Diseases， Taizhou First People′s Hospital in Zhejiang Province， Taizhou   318020， China; 2.Department of Respiratory Medicine， Taizhou First People′s Hospital in Zhejiang Province， Taizhou   318020， China; 3.Department of Gastroenterology， Taizhou First People′s Hospital in Zhejiang Province， Taizhou   318020， China

[Abstract] Objective To explore the intervention effect of microRNA-7 （miR-7） regulated by amino-terminal kinase （JNK）/p38 pathway on colorectal cancer rats induced by helicobacter pylori （Hp） infection. Methods Sixty male SD rats were selected， 15 of them were taken as the normal group， and the other 45 rats were used to establish colorectal cancer models induced by Hp infection， which were randomly divided into model group， up-regulated group and down-regulated group， with 15 rats in each group. The up-regulated group and down-regulated group were transfected with miR-7. The transfection efficiency of miR-7 was identified， the detection rate of each group was compared， and the expression level of Th17/Treg related factors mRNA and JNK/p38 pathway protein were measured. Results Compared with the normal group， the expressions of miR-7， Foxp3， IL-10 were lower in the other three groups， and IL-17A， IL-21， JNK and p38 were higher in the other three groups （P<0.05）. Compared with the model group， the expressions of miR-7， Foxp3 and IL-10 were lower in the down-regulated group， while the expressions of IL-17A， IL-21， JNK and p38 were higher. The expressions of miR-7， Foxp3 and IL-10 were higher in the up-regulated group， while the expression of IL-17A， IL-21， JNK and p38 was lower（P<0.05）. Conclusion Up-regulated miR-7 can improve immunity and slow down the development of colorectal cancer， and its mechanism may be related to JNK/p38 pathway.

[Key words] Colorectal cancer; Helicobacter pylori infection; Terminal kinase; MicroRNA-7

结直肠癌是世界上最常见的恶性肿瘤之一，近年来发病率逐年上升，且死亡率高，故明确直肠癌的发病机制有助于早期的诊治[1-2]。研究表明[3]，幽门螺杆菌（Helicobacter pylori，Hp）是胃腺癌的致癌因子之一，肠道菌群在早期的直肠癌形成中扮演着重要角色。微小RNA-7（MicroRNA-7，miR-7）成熟体由23个核苷酸组成，在肿瘤中具有重要作用，调控肿瘤细胞的生长、侵袭与转移，且miR-7为肿瘤抑制因子，在结直肠癌的发生、发展中起着重要作用[4-5]。JNK具有致癌作用，其活化的强度与持续的时间不同，可使细胞的反应产生不同结果。p38为有丝蛋白激酶家族成员，可调节细胞的增殖。本研究分析基于JNK/p38通路调控miR-7对Hp感染诱导结直肠癌大鼠的干预作用，以明确miR-7与Hp感染诱导的结直肠癌关系，为临床上结直肠癌的诊治提供参考，现报道如下。……