Abstract：
OBJECTIVE: The purpose of the present study was to potential effects of forsythiaside A (FA) on Sjogren\'s syndrome (SS).
METHODS: Enzyme linked immunosorbent assay for detecting cytokines and Western blotting was used for detecting related protein expression.
RESULTS: FA effectively reduced the secretion of inflammatory cytokines, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in SS. FA also effectively inhibited the high expression of Grp78 in SS. When Grp78 expression was silenced, it effectively reduced the secretion of inflammatory cytokines, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in the nucleus in SS. FA effectively inhibit the secretion of inflammatory cytokines induced by overexpression of Grp78, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in the nucleus in SS.
CONCLUSIONS: FA induces the degradation of Grp78 protein, regulates the NF-κB signaling pathway in SS and inhibited NLRP3 inflammasome activation and reduced the release of inflammatory cytokines to alleviate SS.
METHODS: Enzyme linked immunosorbent assay for detecting cytokines and Western blotting was used for detecting related protein expression.
RESULTS: FA effectively reduced the secretion of inflammatory cytokines, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in SS. FA also effectively inhibited the high expression of Grp78 in SS. When Grp78 expression was silenced, it effectively reduced the secretion of inflammatory cytokines, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in the nucleus in SS. FA effectively inhibit the secretion of inflammatory cytokines induced by overexpression of Grp78, the expression of Caspase-1 and NLRP3 proteins and the expression of p65 in the nucleus in SS.
CONCLUSIONS: FA induces the degradation of Grp78 protein, regulates the NF-κB signaling pathway in SS and inhibited NLRP3 inflammasome activation and reduced the release of inflammatory cytokines to alleviate SS.
摘要：
目的：本研究的目的是连翘苷A（FA）对干燥综合征（SS）的潜在影响。
方法：采用酶联免疫吸附法检测细胞因子，采用免疫印迹法检测相关蛋白表达。
结果：FA有效减少了炎性细胞因子的分泌，SS中Caspase-1和NLRP3蛋白的表达和p65的表达。FA还有效抑制了Grp78在SS中的高表达。当Grp78表达沉默时，它有效地减少了炎症细胞因子的分泌，Caspase-1和NLRP3蛋白在SS细胞核中的表达和p65的表达。FA可有效抑制Grp78过表达诱导的炎性细胞因子分泌、Caspase-1和NLRP3蛋白的表达以及SS细胞核中p65的表达。
结论：FA诱导Grp78蛋白降解，调节SS中NF-κB信号通路,抑制NLRP3炎症小体的活化,减少炎症因子的释放,缓解SS。
方法：采用酶联免疫吸附法检测细胞因子，采用免疫印迹法检测相关蛋白表达。
结果：FA有效减少了炎性细胞因子的分泌，SS中Caspase-1和NLRP3蛋白的表达和p65的表达。FA还有效抑制了Grp78在SS中的高表达。当Grp78表达沉默时，它有效地减少了炎症细胞因子的分泌，Caspase-1和NLRP3蛋白在SS细胞核中的表达和p65的表达。FA可有效抑制Grp78过表达诱导的炎性细胞因子分泌、Caspase-1和NLRP3蛋白的表达以及SS细胞核中p65的表达。
结论：FA诱导Grp78蛋白降解，调节SS中NF-κB信号通路,抑制NLRP3炎症小体的活化,减少炎症因子的释放,缓解SS。
