微创医学

目的研究辅助性T细胞22(Th22)及微小RNA-200a（miR-200a）在四氯化碳(CCl4)诱导肝纤维化小鼠模型中的表达及相互关系。方法纳入雄性BALB/c小鼠40只，根据随机数字表法分为模型组(n=20)和对照组(n=20)。对照组腹腔内注射橄榄油，模型组腹腔内注射CCl4溶液建立肝纤维化模型。HE和Masson染色观察小鼠肝脏病理改变，免疫组织化学染色检测肝脏组织中α-平滑肌肌动蛋白(α-SMA)的表达，流式细胞术检测小鼠脾脏Th22细胞数变化，RT-PCR检测肝脏组织IL-22和miR-200a mRNA的表达。结果(1)肝组织病理切片HE染色和Masson染色显示：CCl4腹腔注射法成功建立肝纤维化小鼠模型。(2)模型组α-SMA表达量明显高于对照组（P＜0.05）。（3）模型组小鼠脾脏Th22细胞亚群比例明显高于对照组（P＜0.05）。（4）模型组的肝组织IL-22 mRNA的表达量明显高于对照组，模型组的肝组织miR-200a mRNA的表达量低于对照组（均P＜0.05）。结论CCl4致肝纤维化模型小鼠Th22细胞呈现高表达，miR-200a mRNA呈现低表达，Th22细胞及miR-200a可能参与了肝纤维化的发生发展过程。

ObjectiveTo study the expression and correlation of T helper cells 22 (Th22) and micro RNA 200a（miR-200a）in the mouse model of hepatic fibrosis induced by carbon tetrachloride (CCl4). MethodsA total of 40 male BALB/c mouse were enrolled, and they were assigned to model group (n=20) and control group (n=20) according to the random number table method. The control group was intraperitoneally injected with olive oil, whereas the model group was intraperitoneally injected with CCl4 solution to establish hepatic fibrosis model. The HE and Masson staining were employed to observe hepatic pathological changes of mouse, the immunohistochemical staining to detect the expression of α-smooth muscle actin (α-SMA) in hepatic tissues, the flow cytometry to measure changes of Th22 cells in mouse spleen, and the RT-PCR to examine the mRNA expressions of IL-22 and miR 200a in hepatic tissues. Results(1) The HE and Masson staining of pathological section of hepatic tissues revealed that the mouse model of hepatic fibrosis was successfully established by intraperitoneal injection with CCl4. (2) The model group yielded a significantly higher expression of α-SMA as compared with the control group (P＜0.05). (3) The model group yielded prominently higher proportion of Th22 cells subpopulation in mouse spleen as compared with the control group (P＜0.05). (4) The model group yielded a significantly higher expression of IL-22 mRNA, and a lower expression of miR-200a mRNA in hepatic tissues in the comparison of the control group (all P＜0.05). ConclusionTh22 cells of the mouse model of hepatic fibrosis induced by CCl4 interpret high expressions, whereas miR-200a mRNA present lower expressions, and thus Th22 cells and miR-200a might participate in the occurrence and development of hepatic fibrosis.