论文部分内容阅读
目的研究苹果多糖对小鼠结肠炎癌变的预防作用,并探讨其作用机制。方法从苹果渣中提取苹果多糖,使用致炎剂葡聚糖硫酸钠(DSS)和致癌剂氧化偶氮甲烷(AOM),建立小鼠结肠炎相关结直肠癌动物模型。通过免疫组织化学、蛋白质印迹法、酶联免疫分析等方法观察苹果多糖预防用药对各组小鼠血清中促炎细胞因子肿瘤坏死因子(TNF)-α以及组织TLR4/My D88/NF-κB p65通路的影响。结果苹果多糖预防用药20周后,与模型组(95%致癌率)相比,苹果多糖(1.25%、2.5%和5%)将结直肠肿瘤的发生率降至26%、10%、5%。蛋白质印迹法结果显示,苹果多糖各个剂量组均降低结直肠组织中TLR4、My D88和NF-κB p65蛋白表达。酶联免疫分析结果显示,苹果多糖各剂量组小鼠血清中肿瘤坏死因子-α水平明显降低(P<0.05)。结论苹果多糖可有效预防结肠炎癌变,其作用机制可能与其抑制TLR4/My D88/NF-κB通路有关。
Objective To study the preventive effect of apple polysaccharide on colorectal cancer in mice and to explore its mechanism. Methods The polysaccharides of apple were extracted from apple pomace, and colitis-associated colorectal cancer model was established by using dextran sodium sulfate (DSS) and carcinogen oxidative methylazide (AOM). Immunohistochemistry, Western blotting and enzyme-linked immunosorbent assay were used to observe the effects of polysaccharides from apple polysaccharides on serum levels of pro-inflammatory cytokines TNF-α and TLR4 / My D88 / NF-κB p65 The impact of access. Results Apple polysaccharide (1.25%, 2.5% and 5%) reduced the incidence of colorectal tumor to 26%, 10% and 5% compared with model group (95% carcinogenicity) . Western blotting results showed that the polysaccharide of each dose of polysaccharides reduced the expression of TLR4, My D88 and NF-κB p65 in colorectal tissues. Enzyme-linked immunosorbent assay showed that the levels of TNF-α in the serum of mice treated with polysaccharide of apple polysaccharide were significantly decreased (P <0.05). Conclusion Apple polysaccharides can effectively prevent colorectal carcinogenesis and its mechanism may be related to its inhibition of TLR4 / My D88 / NF-κB pathway.