添加短链脂肪酸的TPN对大鼠晚期结肠癌吻合口愈合的研究

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目的研究添加短链脂肪酸(Short Chain Fatty Acids,SCFA)的全肠外营养(Total Parenteral Nutri-tion,TPN)对晚期结肠癌大鼠模型结肠吻合口愈合的影响。方法应用瘤块转移法建立晚期结肠癌大鼠Ⅰ期结肠吻合模型,随机分为2组①SCFA组,于常规TPN液中添加SCFA②TPN组行常规TPN。术后第6天处死大鼠,标本作病理组织学检查,行肠系膜淋巴结细菌培养,检测黏膜细胞的DNA周期及Ⅰ型胶原蛋白的表达。结果光学显微镜下和透射电镜下均可见SCFA组吻合口胶原纤维粗大、密集,并趋向与肠轴平行排列;对照组结肠黏膜细胞增殖期(S期)百分比(6.23±2.75)显著低于SCFA组(11.57±3.54,P=0.001);Ⅰ型胶原蛋白显示棕黄色颗粒位于细胞浆内,SCFA组表达明显,对照组不明显。对照组肠系膜淋巴结细菌培养的阳性率和菌落计数(1.90±1.06)显著高于SCFA组(0.84±1.14,P=0.025)。结论添加SCFA的TPN能减少肠道菌群易位,保护结肠黏膜的屏障功能,能促进荷瘤状态下大鼠结肠上皮细胞的增殖,增强结肠吻合口的胶原代谢和蛋白质合成,促进Ⅰ型胶原蛋白的表达,促进结肠吻合口的愈合。 Objective To study the effect of total parenteral nutrition (TPN) supplemented with Short Chain Fatty Acids (SCFA) on the healing of colonic anastomosis in a rat model of advanced colon cancer. METHODS: The stage I colon necrosis model of advanced colon cancer was established by tumor mass transfer and divided into 2 groups of 1 SCFA group. Conventional TPN was added to the conventional TPN solution and SCFA2TPN group. On the 6th day after operation, the rats were sacrificed. Histopathological examination of the specimens was performed. Mesenteric lymph node bacterial cultures were performed. The DNA cycle of the mucosal cells and the expression of type I collagen were detected. RESULTS: Under the light microscope and transmission electron microscope, the collagen fibers of the anastomosis in the SCFA group were thick and dense, and they were parallel to the intestinal axis. The percentage of the proliferative phase (S phase) of the colon mucosa in the control group was significantly lower than that of the SCFA group (6.23±2.75). (11.57±3.54, P=0.001); type I collagen showed brown-yellow particles located in the cytoplasm, which was evident in the SCFA group but not in the control group. The positive rate and colony count (1.90±1.06) of the mesenteric lymph nodes in the control group were significantly higher than those in the SCFA group (0.84±1.14, P=0.025). Conclusion TPN with SCFA can reduce the translocation of intestinal flora, protect the barrier function of colonic mucosa, promote the proliferation of rat colonic epithelial cells under tumor-bearing conditions, increase collagen metabolism and protein synthesis in colonic anastomosis, and promote type I collagen. The expression of the protein promotes healing of the anastomotic stoma in the colon.
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