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首页> 外文期刊>Surgical Endoscopy >Enhancement of port site metastasis by hyaluronic acid under CO2 pneumoperitoneum in a murine model.
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Enhancement of port site metastasis by hyaluronic acid under CO2 pneumoperitoneum in a murine model.

机译：透明质酸在鼠模型中CO2气腹下增强端口部位转移。

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BACKGROUND: The mechanism underlying the development and progression of port site metastasis after laparoscopic surgery for cancer is still not understood. Hyaluronic acid secreted from mesothelial cells is thought to be a key factor that causes adhesion between cancer cells and mesothelial cells. Using a murine model of carbon dioxide (CO2) pneumoperitoneum, we evaluated the effect of exogenous hyaluronic acid on port site metastasis. METHODS: BALB/c mice were injected with 5 A- 106 human gastric carcinoma (MKN45) cells and divided into four groups treated with or without hyaluronic acid and with or without pneumoperitoneum. Three weeks later, the frequency and weight of port site metastases were determined. The effects of hyaluronic acid on tumorigenicity and tumor growth were examined in mice subcutaneously injected with MKN45 cells. RESULTS: Port site metastasis occurred significantly less frequently in the pneumoperitoneum-only group than in the pneumoperitoneum-with-hyaluronic-acid group (75% vs 100%, p < 0.05). The port site metastatic tumor weighed significantly less in the control group (anesthesia only) than in the hyaluronic acid group (89 +/- 17 vs 288 +/- 35 mg, p < 0.05); it also weighed less in the pneumoperitoneum-only group than in the pneumoperitoneum-with-hyaluronic-acid group(87 +/- 24 vs 298 +/- 51 mg, p < 0.05). The frequency and weight of tumors in the subcutaneous tissue were not significantly different between groups with or without hyaluronic acid injection (95% vs 90%, 331 +/- 128 vs 322 +/- 115 mg). CONCLUSIONS: Under CO2 pneumoperitoneum, exogenous hyaluronic acid increased the frequency and weight of port site metastasis in a murine model.Hyaluronic acid secreted from mesothelial cells may be associated with the formation of port site metastasis after laparoscopic surgery for cancer under pneumoperitoneum.
机译：背景：腹腔镜手术治疗癌症后港口部位转移的发生和发展的机制仍不清楚。从间皮细胞分泌的透明质酸被认为是引起癌细胞与间皮细胞之间粘附的关键因素。使用二氧化碳（CO2）气腹的小鼠模型，我们评估了外源透明质酸对端口部位转移的影响。方法：BALB / c小鼠注射5 A-106人胃癌（MKN45）细胞，分为四组，分别用或不用透明质酸，不使用气腹膜治疗。三周后，确定端口部位转移的频率和重量。在皮下注射了MKN45细胞的小鼠中检查了透明质酸对致瘤性和肿瘤生长的影响。结果：仅气腹腹膜组与透明质酸肺气腹组相比，发生端口部位转移的频率明显降低（75％vs 100％，p <0.05）。与透明质酸组相比，对照组（仅麻醉）中，移植部位转移性肿瘤的重量明显减轻（89 +/- 17 vs 288 +/- 35 mg，p <0.05）。单纯气腹组的患者的体重也比透明质酸气腹组的患者轻（87 +/- 24 vs 298 +/- 51 mg，p <0.05）。在有或没有透明质酸注射的组之间，皮下组织中肿瘤的频率和重量没有显着差异（95％vs 90％，331 +/- 128 vs 322 +/- 115 mg）。结论：在CO2气腹下，外源性透明质酸增加了鼠模型中端口位转移的频率和重量;腹腔镜手术治疗气腹下癌症后，间皮细胞分泌的透明质酸可能与端口位转移的形成有关。

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