Abstract：
BACKGROUND: Based on the core pathogenesis of hepatosplenic disorder and qi transformation disorder in ulcerative colitis, Tong-Xie-Yao-Fang (TXYF) is a classical traditional Chinese medicine commonly used to treat ulcerative colitis. Our study revealed that it has the potential to prevent colitis-associated colorectal cancer, which embodies the academic concept in traditional Chinese medicine of treating the disease before it develops.
OBJECTIVE: This study was aimed at evaluating the therapeutic role of TXYF in treating colitis-associated colorectal cancer and exploring its possible underlying mechanisms.
METHODS: A colitis-associated colorectal cancer model was established in mice using azoxymethane and dextran sulfate sodium salt to examine the therapeutic effect of TXYF. The mouse body weights were observed. Hematoxylin-eosin staining was used to evaluate mouse colon histopathology. Colon cancer cells and colon epithelial cells were used to explore the potential molecular mechanisms. The proliferation and apoptosis of cells were detected by CCK8 and cell colony assays, flow cytometry and western blotting. The epithelial-mesenchymal transition (EMT) and mitophagy markers were examined by immunohistochemistry, western blotting, quantitative real-time PCR and immunofluorescence staining.
RESULTS: TXYF inhibited the tumorigenesis of mice with colitis-associated colorectal cancer and the growth of inflammatory colon cells. TXYF induced mitophagy in colon cancer cells through the PTEN-induced putative kinase 1 (PINK1)/Parkin pathway to reverse EMT, which was consistent with the results in mice with colitis-associated colorectal cancer.
CONCLUSIONS: The results of the present study demonstrated that TXYF effectively inhibited the progression of colitis-associated colorectal cancer through the PINK1/Parkin pathway, which provides new evidence for prevention strategies for this disease.
OBJECTIVE: This study was aimed at evaluating the therapeutic role of TXYF in treating colitis-associated colorectal cancer and exploring its possible underlying mechanisms.
METHODS: A colitis-associated colorectal cancer model was established in mice using azoxymethane and dextran sulfate sodium salt to examine the therapeutic effect of TXYF. The mouse body weights were observed. Hematoxylin-eosin staining was used to evaluate mouse colon histopathology. Colon cancer cells and colon epithelial cells were used to explore the potential molecular mechanisms. The proliferation and apoptosis of cells were detected by CCK8 and cell colony assays, flow cytometry and western blotting. The epithelial-mesenchymal transition (EMT) and mitophagy markers were examined by immunohistochemistry, western blotting, quantitative real-time PCR and immunofluorescence staining.
RESULTS: TXYF inhibited the tumorigenesis of mice with colitis-associated colorectal cancer and the growth of inflammatory colon cells. TXYF induced mitophagy in colon cancer cells through the PTEN-induced putative kinase 1 (PINK1)/Parkin pathway to reverse EMT, which was consistent with the results in mice with colitis-associated colorectal cancer.
CONCLUSIONS: The results of the present study demonstrated that TXYF effectively inhibited the progression of colitis-associated colorectal cancer through the PINK1/Parkin pathway, which provides new evidence for prevention strategies for this disease.
摘要：
背景：基于溃疡性结肠炎肝脾障碍和气转化障碍的核心发病机制，通解药方（TXYF）是一种常用于治疗溃疡性结肠炎的传统中药。我们的研究表明，它有可能预防结肠炎相关的结直肠癌，这体现了中医治病未病的学术理念。
目的：本研究旨在评估TXYF治疗结肠炎相关性结直肠癌的作用，并探讨其可能的潜在机制。
方法：使用氧化偶氮甲烷和葡聚糖硫酸钠盐在小鼠中建立结肠炎相关的结直肠癌模型，以检查TXYF的治疗效果。观察小鼠体重。苏木精-伊红染色用于评估小鼠结肠组织病理学。结肠癌细胞和结肠上皮细胞用于探索潜在的分子机制。CCK-8和细胞集落试验检测细胞的增殖和凋亡,流式细胞术和蛋白质印迹。通过免疫组织化学检查上皮-间质转化（EMT）和线粒体自噬标志物，西方印迹,实时定量PCR和免疫荧光染色。
结果：TXYF抑制结肠炎相关性结直肠癌小鼠的肿瘤发生和炎性结肠细胞的生长。TXYF通过PTEN诱导的推定激酶1（PINK1）/Parkin通路逆转EMT诱导结肠癌细胞的线粒体自噬，这与结肠炎相关结直肠癌小鼠的结果一致。
结论：本研究的结果表明，TXYF通过PINK1/Parkin通路有效抑制结肠炎相关性结直肠癌的进展，这为这种疾病的预防策略提供了新的证据。
目的：本研究旨在评估TXYF治疗结肠炎相关性结直肠癌的作用，并探讨其可能的潜在机制。
方法：使用氧化偶氮甲烷和葡聚糖硫酸钠盐在小鼠中建立结肠炎相关的结直肠癌模型，以检查TXYF的治疗效果。观察小鼠体重。苏木精-伊红染色用于评估小鼠结肠组织病理学。结肠癌细胞和结肠上皮细胞用于探索潜在的分子机制。CCK-8和细胞集落试验检测细胞的增殖和凋亡,流式细胞术和蛋白质印迹。通过免疫组织化学检查上皮-间质转化（EMT）和线粒体自噬标志物，西方印迹,实时定量PCR和免疫荧光染色。
结果：TXYF抑制结肠炎相关性结直肠癌小鼠的肿瘤发生和炎性结肠细胞的生长。TXYF通过PTEN诱导的推定激酶1（PINK1）/Parkin通路逆转EMT诱导结肠癌细胞的线粒体自噬，这与结肠炎相关结直肠癌小鼠的结果一致。
结论：本研究的结果表明，TXYF通过PINK1/Parkin通路有效抑制结肠炎相关性结直肠癌的进展，这为这种疾病的预防策略提供了新的证据。
