机构地区:[1]北京市通州区120紧急救援中心,101100 [2]包头医学院第二附属医院普通外科
出 处:《实用肝脏病杂志》2021年第4期476-479,共4页Journal of Practical Hepatology
基 金:北京市自然科学基金资助项目(编号:20198485)。
摘 要:目的研究灵芝多糖对HepG2细胞诱导的肝癌小鼠肠道菌群及其菌群代谢功能的调节作用。方法采用HepG2细胞构建肝癌小鼠模型,将21只造模成功的肝癌小鼠随机分为模型组、灵芝多糖(GLP)和益生菌处理组,每组7只,另选择正常小鼠7只作为对照组,给予药物处理组动物GLP或益生菌灌胃,另两组采用生理盐水灌胃,连续干预2 w。采用镜检法和变性梯度凝胶电泳法(DGGE)检测小鼠肠道菌群结构、多样性及其脂肪酸代谢产物水平。结果肝癌小鼠肠道双歧杆菌、乳酸杆菌、大肠埃希菌和肠球菌数量分别为(2.3±0.5)×10^(10) CFU/g、(12.2±2.2)×10^(9) CFU/g、(3.9±1.5)×10^(7) CFU/g和(5.0±1.2)×10^(10) CFU/g,显著高于对照组[分别为(0.94±0.18)×10^(10) CFU/g、(3.49±0.66)×10^(9) CFU/g、(1.12±0.11)×107 CFU/g和(0.57±0.06)×10^(10) CFU/g,P<0.05],GLP干预组小鼠肠道上述菌群分别为(1.1±0.1)×10^(10) CFU/g、(6.5±1.1)×10^(9) CFU/g、(1.8±0.2)×107 CFU/g和(1.5±0.1)×10^(10) CFU/g,均显著低于模型组(P<0.05);GLP处理组小鼠肠道菌群丰富度、多样性指数和均匀度分别为(7.2±1.1)S、(4.8±1.1)H和(1.0±0.2)E,显著高于模型组[分别为(5.7±1.2)S、(3.4±0.5)H、(0.7±0.1)E,P<0.05];GLP干预组小鼠肠道菌群乙酸、丙酸、正丁酸和D-乳酸水平分别为(37.9±3.3)mmol/L、(3.9±0.2)mmol/L、(2.3±0.3)mmol/L和(0.2±0.0)g/L,与模型组[分别为(26.8±3.2)mmol/L、(1.8±0.4)mmol/L、(1.8±0.2)mmol/L和(0.5±0.1)g/L比,差异显著(P<0.05)]。结论肝癌小鼠肠道菌群出现了失调,而应用GLP可能帮助改善机体肠道微生态紊乱状态,其意义还有待探讨。Objective The aim of this experimental study was to implore the regulation of intestinal floras and their metabolism functions by ganoderma lucidum plysaceharide(GLP)in mice with HepG2 cell-induced implanted cancer.Methods The subcutaneous cancer in mice was established by HepG2 cell implantation,and 21 mice with successful implanted cancer were randomly divided into model,GLP-intervened and probiotics-intervened groups,with 7 in each.7 normal mice were selected as control.The GLP and probiotics were administered intragastrically,while normal saline were given by gavage in model and control for 2 weeks.The diversity of intestinal floras,and fatty acid metabolites were detected by microscopy and denaturing gradient gel electrophoresis(DGGE).Results The number of Bifidobacterium,Lactobacillus,Escherichia Coli and Enterococcus in model group were(2.3±0.5)×10^(10) CFU/g,(12.2±2.2)×10^(9) CFU/g,(3.9±1.5)×107 CFU/g and(5.0±1.2)×10^(10) CFU/g,all significantly higher than[(0.94±0.18)×10^(10) CFU/g,(3.49±0.66)×10^(9) CFU/g,(1.12±0.11)×107 CFU/g and(0.57±0.06)×10^(10) CFU/g,respectively,P<0.05]in the control,ylajj@163.com while they were(1.1±0.1)×10^(10) CFU/g,(6.5±1.1)×10^(9) CFU/g,(1.8±0.2)×107 CFU/g and(1.5±0.1)×10^(10) CFU/g in GLP-intervened group(P<0.05);the abundance,the diversity index and uniformity of intestinal floras in GLP-intervened group were(7.2±1.1)S,(4.8±1.1)H and(1.0±0.2)E,all significantly higher than[(5.7±1.2)S,(3.4±0.5)H and(0.7±0.1)E,respectively,P<0.05]in the model;the intestinal flora acetic acid,propionic acid and n-butyric acid in GLP-intervened group were(37.9±3.3)mmol/L,(3.9±0.2)mmol/L and(2.3±0.3)mmol/L,all significantly higher than[(26.8±3.2)mmol/L,(1.8±0.4)mmol/L and(1.8±0.2)mmol/L,respectively,P<0.05],while the D-lactic acid was(0.2±0.0)g/L,much lower than(0.5±0.1)g/L in the model(P<0.05).Conclusion The imbalance of intestinal floras is closely related to the carcinogenesis in mice,and the GLP administration might correct the intestinal microecological
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