The study of oral streptococcal pathogenicity of autoimmune hepatitis

本研究分析了ILY诱导胆管上皮细胞钙振荡与上述现象之间的可能关系，以探讨ILY诱导胆管上皮细胞钙振荡的分子机制。通过对加载Fura-2的细胞进行钙成像分析来分析细胞内游离钙。ILY处理细胞后，细胞核内游离钙含量增加，随后内质网面积明显增加。钙调磷酸酶抑制剂环孢素A阻止ILY诱导的钙调磷酸酶/NFAT 1激活，细胞死亡和钙振荡。浓度为10-40 ng/ ml的ILY能够诱导钙振荡，激活钙调磷酸酶/NFAT 1信号通路;灭活PI 3 K/ AKT/ MTOR通路，并引起ER应激障碍，导致HuCCT 1细胞中的非凋亡性细胞死亡。

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.