目的 探究E-钙黏蛋白（E-cad）过表达对血吸虫感染引起的肝组织上皮间质转化（EMT）和纤维化的影响。 方法 16只小鼠随机分为E-cad组和对照组，分别经尾静脉注射2 × 10¹¹ vg的腺相关病毒8包装的E-cad质粒和空质粒。注射后3周，经腹部贴片法感染日本血吸虫尾蚴[（20 ± 1）条/只]，感染后6周取肝组织。提取肝组织RNA，qPCR检测目的基因的相对转录水平。提取肝组织蛋白，蛋白质免疫印迹（Western blotting）检测目的蛋白的相对表达水平。肝组织石蜡切片行苏木精-伊红（HE）染色和Masson染色，计算单个虫卵肉芽肿面积和胶原纤维面积。使用GraphPad Prism 9软件进行统计学分析，两组比较采用t检验。 结果 对照组和E-cad组小鼠肝组织中E-cad的mRNA相对转录水平分别为1.15 ± 0.07、7.19 ± 2.43，E-cad的蛋白相对表达水平分别为1.03 ± 0.16、1.42 ± 0.22，E-cad组均高于对照组（t = 4.30、3.62，P < 0.05、0.01），肝脏过表达E-cad小鼠模型构建成功。qPCR结果显示，E-cad组小鼠肝组织中波形蛋白（Vim）、α-平滑肌肌动蛋白（α-SMA）、Ⅰ型胶原蛋白（Col-1）和Ⅲ型胶原蛋白（Col-3）的mRNA相对转录水平分别为0.60 ± 0.17、0.62 ± 0.19、0.31 ± 0.17、0.30 ± 0.13，均低于对照组的1.37 ± 0.33、1.43 ± 0.35、1.78 ± 0.84、1.78 ± 0.45（t = 3.60、3.48、3.74、5.52，P < 0.05、0.05、0.05、0.01）。Western blotting结果显示，E-cad组小鼠肝组织中Vim、N-钙黏蛋白（N-cad）、α-SMA、Col-1、Col-3、转化生长因子β1（TGF-β1）、Samd2和Smad3的蛋白相对表达水平分别为0.22 ± 0.13、0.37 ± 0.14、0.29 ± 0.19、0.23 ± 0.06、0.17 ± 0.02、0.32 ± 0.13、0.57 ± 0.14和0.54 ± 0.10，均低于对照组的0.71 ± 0.13、0.65 ± 0.08、0.81 ± 0.13、0.43 ± 0.08、0.50 ± 0.16、0.68 ± 0.07、0.87 ± 0.04、0.82 ± 0.06（t = 4.39、2.75、3.91、3.99、3.47、3.92、2.95、4.61，P < 0.01、0.05、0.01、0.01、0.05、0.01、0.05、0.05）。HE染色显示，对照组和E-cad组小鼠的肝组织单卵肉芽肿面积分别为[（34.10 ± 6.94） ×10⁴]和[（12.76 ± 3.16） × 10⁴]μm²；Masson染色显示，对照组和E-cad组小鼠的肝组织单卵肉芽肿胶原纤维面积分别为[（8.50 ± 2.36） × 10⁴]和[（3.65 ± 0.90） × 10⁴]μm²。E-cad组的单卵肉芽肿面积和胶原纤维面积均小于对照组（t = 7.41、5.01，均P < 0.01）。 结论 小鼠肝脏过表达E-cad能够减轻日本血吸虫感染引起的肝脏EMT和纤维化水平，这一过程可能通过抑制TGF-β1/Smad信号通路而实现。

Objective To investigate the impact of E-cadherin (E-cad) overexpression on hepatic epithelial-mesenchymal transition (EMT) and liver fibrosis induced by Schistosoma japonicum infection. Methods A total of 16 mice were randomly divided into the E-cad group and the control group, and were injected with 2 × 10¹¹ vector genomes of E-cad plasmid or empty plasmid packaged with adeno-associated virus 8 via the tail vein. All mice were infected with S. japonicum cercariae [(20 ± 1) per mouse] via the abdomen 3 weeks post-injection, and liver tissues were collected 6 weeks post-infection. Total RNA was extracted from liver tissues, and the relative transcription levels of target genes were detected with a real-time quantitative PCR (qPCR) assay. Total protein was extracted from liver tissues, and the relative expression of target proteins was detected using Western blotting. Paraffin-embedded liver sections were stained with hematoxylin and eosin (HE) and Masson’s trichrome stains to assess the area of single-egg granulomas and collagen fibers. All statistical analyses were performed using the software GraphPad Prism 9, and differences of means between groups were assessed using t-test. Results The relative mRNA transcription levels of E-cad were 1.15 ± 0.07 and 7.19 ± 2.43 in mouse liver tissues in the control and E-cad group (t = 4.30, P < 0.05), and the relative protein expression of E-cad were 1.03 ± 0.16 and 1.42 ± 0.22 in the control and E-cad group (t = 3.62, P < 0.01), indicating successful modeling of hepatic E-cad overexpression in mice. qPCR assay quantified lower relative mRNA transcription of vimentin (Vim) [(0.60 ± 0.17) vs. (1.37 ± 0.33); t = 3.60, P < 0.05], α-smooth muscle actin (α-SMA) [(0.62 ± 0.19) vs. (1.43 ± 0.35); t = 3.48, P < 0.05], collagenⅠ (Col-1) [(0.31 ± 0.17) vs. (1.78 ± 0.84); t = 3.74, P < 0.05] and collagenⅢ (Col-3) [(0.30 ± 0.13) vs. (1.78 ± 0.45); t = 5.52, P < 0.01] in mouse liver tissues in the E-cad group than in the control group, and Western blotting determined lower relative expression of Vim [(0.22 ± 0.13) vs. (0.71 ± 0.13); t = 4.39, P < 0.01], N-cadherin (N-cad) [(0.37 ± 0.14) vs. (0.65 ± 0.08); t = 2.75, P < 0.05], α-SMA [(0.29 ± 0.19) vs. (0.81 ± 0.13); t = 3.91, P < 0.01], Col-1 [(0.23 ± 0.06) vs. (0.43 ± 0.08); t = 3.99, P < 0.01], Col-3 [(0.17 ± 0.02) vs. (0.50 ± 0.16); t = 3.47, P < 0.05], transforming growth factor-β1 (TGF-β1) [(0.32 ± 0.13) vs. (0.68 ± 0.07); t = 3.92, P < 0.01], Smad2 [(0.57 ± 0.14) vs. (0.87 ± 0.04); t = 2.95, P < 0.05] and Smad3 [(0.54 ± 0.10) vs. (0.82 ± 0.06); t = 4.61, P < 0.05] in mouse liver tissues in the E-cad group than in the control group. HE staining showed that the area of single-egg liver granulomas were [(34.10 ± 6.94) × 10⁴] and [(12.76 ± 3.16) × 10⁴] μm² in the control and E-cad groups (t = 7.41, P < 0.01), and Masson staining showed that the areas of collagen fibers with single-egg liver granulomas were [(8.50 ± 2.36) × 10⁴] and [(3.65 ± 0.90) × 10⁴] μm² in the control and E-cad groups (t = 5.01, P < 0.01), respectively. Conclusion Hepatic E-cad overexpression alleviates EMT and liver fibrosis induced by S. japonicum infection in mice, potentially through inhibition of the TGF-β1/Smad signaling pathway.