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首页> 外文期刊>Biological chemistry >Geniposide alleviates lipopolysaccharide (LPS)-induced inflammation by downregulation of miR-27a in rat pancreatic acinar cell AR42J
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Geniposide alleviates lipopolysaccharide (LPS)-induced inflammation by downregulation of miR-27a in rat pancreatic acinar cell AR42J

机译:Geniposide通过大鼠胰腺缩醛细胞AR42J中的miR-27a的下调减轻了脂多糖(LPS)诱导的炎症

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Pancreatitis is a disease caused by inflammation of pancreatic acinar cells. Geniposide (GEN) possesses anti-inflammation activities. Hence, we investigated the effects of GEN on lipopolysaccharide (LPS)-stimulated AR42J cells. AR42J cells were stimulated by LPS and then treated with GEN and/or transfected with miR-27a mimic or negative control. Cell viability and cell apoptosis were detected using the Cell Counting Kit-8 and flow cytometry, respectively. All related proteins were measured by Western blot. The expression of miR-27a was detected by quantitative real time-polymerase chain reaction (qRT-PCR). Moreover, the expression of inflammatory cytokines inter-leukin-6 (IL-6) and monocyte chemoattractant protein (MCP)-l was analyzed by qRT-PCR and Western blot. LPS significantly decreased cell viability, and enhanced cell apoptosis and IL-6, MCP-1 expression. Then GEN administration alleviated inflammatory injury by increasing cell viability, while reducing apoptosis, and IL-6 and MCP-1 expression. GEN downregulated miR-27a expression which was induced by LPS. Transfection with miR-27a mimic partially eliminated the protective effects of GEN. The phosphorylation of INK and c-Iun was downregulated by GEN while upregulated by miR-27a overexpression. GEN alleviates LPS-induced AR42I cell injury as evidenced by promoting cell growth, and upregulation of IL-6 and MCP-1. This process might be modulated by down-regulating miR-27a and inactivation of INK pathway.
机译:胰腺炎是一种由胰腺腺体细胞炎症引起的疾病。 Geniposide(Gen)具有抗炎活动。因此,我们研究了Gen对脂多糖(LPS)刺激的AR42J细胞的影响。通过LPS刺激AR42J细胞,然后用Gen处理和/或用miR-27a模拟或阴性对照进行处理。使用细胞计数试剂盒-8和流式细胞术检测细胞活力和细胞凋亡。所有相关蛋白质通过蛋白质印迹测量。通过定量实时聚合酶链反应(QRT-PCR)检测miR-27a的表达。此外,通过QRT-PCR和Western印迹分析了炎症细胞因子细胞内-6(IL-6)和单核细胞化学蛋白(MCP)-L的表达。 LPS显着降低细胞活力,增强细胞凋亡和IL-6,MCP-1表达。然后通过增加细胞活力,同时减少细胞凋亡,以及IL-6和MCP-1表达,因此通过增加炎症损伤而减轻了炎症损伤。 Gen下调MiR-27A表达,由LPS诱导。用miR-27a转染模仿部分消除了Gen的保护作用。墨水和C-IUN的磷酸化通过Gen下调,而MiR-27a过表达上调。根据促进细胞生长和UL-6和MCP-1的上调,Gen减轻了LPS诱导的AR42I细胞损伤。该过程可以通过向下调节miR-27a和墨水途径的灭活来调节。

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