The study of oral streptococcal pathogenicity of autoimmune hepatitis

在本研究中，我们分析了钙振荡与各种现象之间的可能关系，以找出ILY诱导的胆管上皮细胞的分子机制。通过对负载Fura-2的细胞进行钙离子成像分析，分析细胞内游离钙浓度。ILY处理组细胞胞核内游离钙离子首先增加，随后内质网面积明显增加。钙调神经磷酸酶抑制剂环孢素A可阻止ILY诱导的钙调神经磷酸酶/NFAT1激活、细胞死亡和钙振荡。在10~40 ng/ml浓度范围内，钙调神经磷酸酶/NFAT1信号通路激活，PI3K/AKT/MTOR通路失活，导致内质网应激障碍，导致HuCCT1细胞非凋亡性死亡。

In the present study we analyzed possible relationship between calcium oscillations and each phenomenon in order to find out the molecular mechanisms in ILY-induced bile duct epithelial cells. Intracellular free calcium was analyzed by performing calcium imaging analysis of Fura-2 loaded cells. Increased free calcium was initially detected in the nuclei of ILY-treated cells subsequently followed with markedly increase in ER area. Calcineurin inhibitor cyclosporine A prevented ILY-induced calcineurin/ NFAT1 activation, cell death, and calcium oscillations. ILY in concentration of 10-40 ng/ ml capable of inducing calcium oscillations, activation of calcineurin/ NFAT1 signalling pathway ; inactivation of PI3K/ AKT/ MTOR pathway, and caused ER stress disorder resulted non-apoptotic cell death in HuCCT1 cells.