益生菌对非酒精性脂肪肝相关细胞的作用
投稿时间:2018-01-21  修订日期:2018-07-11  点此下载全文
引用本文:王斌,蔡敏,黄玲,姜子廷,童敏思,李力.益生菌对非酒精性脂肪肝相关细胞的作用[J].药学实践杂志,2018,36(5):409~416
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作者单位
王斌 同济大学附属杨浦医院消化科, 上海 200090 
蔡敏 同济大学附属杨浦医院消化科, 上海 200090 
黄玲 同济大学附属杨浦医院消化科, 上海 200090 
姜子廷 同济大学附属杨浦医院消化科, 上海 200090 
童敏思 同济大学附属杨浦医院消化科, 上海 200090 
李力 同济大学附属杨浦医院消化科, 上海 200090 
中文摘要:目的 探讨益生菌对非酒精性脂肪肝相关的肠上皮细胞、肝Kupper细胞和肝实质细胞的作用及其作用机制。方法 将人肠上皮细胞Caco-2、大鼠肝Kupper细胞和小鼠肝实质细胞AML12分别分成空白对照组、脂多糖(LPS)组、嗜酸乳杆菌组、LPS+嗜酸乳杆菌组、粪肠球菌组、LPS+粪肠球菌组、双歧杆菌组、LPS+双歧杆菌组,孵育培养6 h。分别检测人肠上皮细胞Caco-2紧密连接相关因子表达情况及细胞通透性、大鼠肝Kupper细胞功能表型相关因子和IκB及p-IκB变化水平、小鼠肝实质细胞AML12脂代谢基因水平和脂类吸收情况。结果 益生菌可显著抑制由LPS刺激引起的人肠上皮细胞Caco-2紧密连接相关因子Occludin、Claudin-1、JAM、ZO-1表达的下降和细胞通透性的增加;明显抑制LPS刺激引起的大鼠肝Kupper细胞表达TNF-α、IFN-γ和IL-6的增加,同时抑制IL-4、IL-10、IL-13的降低和p-IκB蛋白表达的增加;显著抑制由LPS刺激引起的小鼠肝实质细胞AML12脂代谢基因ACACA、SREBF1、FAS、FABP3、FABP4、DGAT1的上调和脂类吸收的增加。结论 益生菌可以通过促进肠上皮细胞紧密连接相关因子的表达,降低细胞通透性,抑制肝Kupper细胞NF-κB通路活性,降低促炎性细胞因子、增加抑炎性细胞因子表达水平,抑制肝实质细胞脂代谢基因表达和脂类吸收等多种途径,保护非酒精性脂肪肝。
中文关键词:非酒精性脂肪肝  益生菌  Caco-2细胞  细胞通透性  Kupffer细胞  p-IκB  AML12细胞  脂类吸收
 
Role of probiotics on nonalcoholic fatty liver disease related cells
Abstract:Objective To explore the effects and mechanisms of probiotics on nonalcoholic fatty liver disease related intestinal epithelial cells, Kupffer cells and liver parenchymal cells. Methods Human intestinal epithelial cells Caco-2, rat Kupffer cells and mouse liver parenchymal cell AML12 were divided into eight groups respectively:the control group, LPS group, Lactobacillus acidophilus group, LPS+Lactobacillus acidophilus group, Enterococcus faecalis group, LPS+Enterococcus faecalis group, Bifidobacterium group and LPS+Bifidobacterium group. All cells were incubated for 6 h and collected to detect the expression of tight junction related factors and cell permeability of human intestinal epithelial cells Caco-2, the levels of functional factors, IκB and p-IκB of rat Kupffer cells, the expression of lipid metabolism genes and lipid absorption of hepatocytes AML12. Results Probiotics significantly inhibited the expression of Occludin, Claudin-1, JAM, ZO-1 and cell permeability induced by LPS in human intestinal epithelial cells Caco-2. Probiotics decreased the levels of TNF-α, IFN-γ, IL-6 and increased the levels of IL-4, IL-10, IL-13 caused by LPS in rat Kupffer cells. The protein level of p-IκB was also inhibited by probiotics. In addition, probiotics significantly inhibited the upregulation of ACACA, SREBF1, FAS, FABP3, FABP4, DGAT1 and lipid absorption induced by LPS in mouse liver parenchymal cells AML12. Conclusion Probiotics can protect nonalcoholic fatty liver disease through promoting the expression of intestinal epithelial tight junction related factors, reducing epithelial cells permeability, inhibiting the activity of NF-κB pathway to decrease the expression of proinflammatory cytokines and increase the levels of anti-inflammatory cytokines in Kuffer cells, inhibiting lipid metabolism genes expression and lipid absorption of hepatocytes.
keywords:nonalcoholic fatty liver disease  probiotics  Caco-2  cell permeability  Kupffer cell  p-IκB  AML12  lipid absorption
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