目的:观察黄芪甲甙干预的病毒性心肌炎(viral myocarditis,VMC)小鼠中TL1A表达的影响,探讨黄芪甲甙治疗VMC的作用机制。方法:取Balb/c小鼠100只,随机分成6组。非感染小鼠腹腔无菌注射不含病毒的Eagle’s培养液0.1 m L,分为正常对照组10...目的:观察黄芪甲甙干预的病毒性心肌炎(viral myocarditis,VMC)小鼠中TL1A表达的影响,探讨黄芪甲甙治疗VMC的作用机制。方法:取Balb/c小鼠100只,随机分成6组。非感染小鼠腹腔无菌注射不含病毒的Eagle’s培养液0.1 m L,分为正常对照组10只,以羧甲基纤维素钠0.1 m L灌胃7 d;高剂量对照组10只,9%黄芪甲甙0.1 m L灌胃7 d;余80只小鼠以腹腔无菌注射0.1 m L内含1×102 5 0%组织感染率(TCID50)柯萨奇病毒B3(Cox sachiev ir us B3,CVB3)的Eagle’s培养液制作VMC模型。VMC小鼠随机分为心肌炎对照组和低、中、高剂量干预组,分别以生理盐水和1%,3%,9%黄芪甲甙[分别为0.07,0.2,0.6 g/(kg.d)]0.1 m L灌胃7 d(每组20只)。14 d后处死全部小鼠并取其心脏。采用RT-PCR及免疫组织化学分别检测心肌TL1A m RNA及蛋白表达水平。结果:正常对照组和高剂量对照组无小鼠死亡,心肌炎对照组有大量小鼠死亡,死亡率为45%(9/20),低、中、高剂量干预组小鼠死亡率分别为30%(6/20),25%(5/20),10%(2/20),高剂量干预组小鼠死亡率较心肌炎对照组明显降低(P<0.05),而低、中剂量干预组小鼠死亡率与心肌炎对照组比较,差异无统计学意义(P>0.05);正常对照组和高剂量对照组心肌未见任何病理改变,然而两组心肌中均有一定量的TL1A mRNA及蛋白表达,两组比较差异无统计学意义(P>0.05),心肌炎对照组TL1A mRNA及蛋白表达水平明显增加,与正常对照组比较,差异有统计学意义(P<0.01),心肌炎小鼠经不同剂量黄芪甲甙干预后,与对照组相比,在高剂量干预组显著下降(P<0.01),而低、中剂量黄芪甲甙对心肌炎小鼠TL1A mRNA、蛋白表达水平以及心肌病变积分无明显影响(P>0.05)。结论:黄芪甲甙治疗VMC可能通过抑制炎症介质、降低TL1A的表达而起作用。展开更多
Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. The host microbiome, as well as viruses and fungi, play important ro...Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. The host microbiome, as well as viruses and fungi, play important roles in the development of IBD either by causing inflammation directly or indirectly through an altered immune system. New technologies have allowed researchers to be able to quantify the various components of the microbiome, which will allow for future developments in the etiology of IBD. Various components of the mucosal immune system are implicated in the pathogenesis of IBD and include intestinal epithelial cells, innate lymphoid cells, cells of the innate (macrophages/monocytes, neutrophils, and dendritic cells) and adaptive (T-cells and B-cells) immune system, and their secreted mediators (cytokines and chemokines). Either a mucosal susceptibility or defect in sampling of gut luminal antigen, possibly through the process of autophagy, leads to activation of innate immune response that may be mediated by enhanced toll-like receptor activity. The antigen presenting cells then mediate the differentiation of naïve T-cells into effector T helper (Th) cells, including Th1, Th2, and Th17, which alter gut homeostasis and lead to IBD. In this review, the effects of these components in the immunopathogenesis of IBD will be discussed.展开更多
文摘目的:观察黄芪甲甙干预的病毒性心肌炎(viral myocarditis,VMC)小鼠中TL1A表达的影响,探讨黄芪甲甙治疗VMC的作用机制。方法:取Balb/c小鼠100只,随机分成6组。非感染小鼠腹腔无菌注射不含病毒的Eagle’s培养液0.1 m L,分为正常对照组10只,以羧甲基纤维素钠0.1 m L灌胃7 d;高剂量对照组10只,9%黄芪甲甙0.1 m L灌胃7 d;余80只小鼠以腹腔无菌注射0.1 m L内含1×102 5 0%组织感染率(TCID50)柯萨奇病毒B3(Cox sachiev ir us B3,CVB3)的Eagle’s培养液制作VMC模型。VMC小鼠随机分为心肌炎对照组和低、中、高剂量干预组,分别以生理盐水和1%,3%,9%黄芪甲甙[分别为0.07,0.2,0.6 g/(kg.d)]0.1 m L灌胃7 d(每组20只)。14 d后处死全部小鼠并取其心脏。采用RT-PCR及免疫组织化学分别检测心肌TL1A m RNA及蛋白表达水平。结果:正常对照组和高剂量对照组无小鼠死亡,心肌炎对照组有大量小鼠死亡,死亡率为45%(9/20),低、中、高剂量干预组小鼠死亡率分别为30%(6/20),25%(5/20),10%(2/20),高剂量干预组小鼠死亡率较心肌炎对照组明显降低(P<0.05),而低、中剂量干预组小鼠死亡率与心肌炎对照组比较,差异无统计学意义(P>0.05);正常对照组和高剂量对照组心肌未见任何病理改变,然而两组心肌中均有一定量的TL1A mRNA及蛋白表达,两组比较差异无统计学意义(P>0.05),心肌炎对照组TL1A mRNA及蛋白表达水平明显增加,与正常对照组比较,差异有统计学意义(P<0.01),心肌炎小鼠经不同剂量黄芪甲甙干预后,与对照组相比,在高剂量干预组显著下降(P<0.01),而低、中剂量黄芪甲甙对心肌炎小鼠TL1A mRNA、蛋白表达水平以及心肌病变积分无明显影响(P>0.05)。结论:黄芪甲甙治疗VMC可能通过抑制炎症介质、降低TL1A的表达而起作用。
基金Supported by NIH KO8 DK093578CCFA Career Development Award 3467(DQS)F Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute
文摘Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. The host microbiome, as well as viruses and fungi, play important roles in the development of IBD either by causing inflammation directly or indirectly through an altered immune system. New technologies have allowed researchers to be able to quantify the various components of the microbiome, which will allow for future developments in the etiology of IBD. Various components of the mucosal immune system are implicated in the pathogenesis of IBD and include intestinal epithelial cells, innate lymphoid cells, cells of the innate (macrophages/monocytes, neutrophils, and dendritic cells) and adaptive (T-cells and B-cells) immune system, and their secreted mediators (cytokines and chemokines). Either a mucosal susceptibility or defect in sampling of gut luminal antigen, possibly through the process of autophagy, leads to activation of innate immune response that may be mediated by enhanced toll-like receptor activity. The antigen presenting cells then mediate the differentiation of naïve T-cells into effector T helper (Th) cells, including Th1, Th2, and Th17, which alter gut homeostasis and lead to IBD. In this review, the effects of these components in the immunopathogenesis of IBD will be discussed.
