论文部分内容阅读
目的:研究大黄素对IFN-和LPS刺激的人结肠癌细胞株HT-29细胞的ERK、JNK和p38 MARK和IL-8表达的影响。方法:人结肠癌细胞株HT-29细胞与40 ng/mL的IFN-共培养12 h,再加入100 ng/mL LPS刺激15 min,用大黄素预处理进行干预。ELISA检测HT-29细胞内的ERK、JNK和p38 MARK含量和细胞上清IL-8含量。结果:IFN-γ和LPS刺激后HT-29细胞的ERK、JNK和p38 MARK磷酸化水平和IL-8分泌明显升高。大黄素对p38和JNK磷酸化有明显的抑制作用,而对ERK磷酸化则没有明显抑制作用;大黄素能显著降低IFN-γ+LPS所引起的HT-29细胞IL-8的大量产生,并且呈明显的剂量依赖关系。结论:大黄素能有效抑制IFN-γ+LPS所引起的HT-29细胞p38和JNK的磷酸化,并显著降低IL-8分泌。
AIM: To investigate the effects of emodin on the expression of ERK, JNK, p38 MARK and IL-8 in human colon cancer cell line HT-29 stimulated by IFN- and LPS. Methods: Human colon cancer cell line HT-29 cells were co-cultured with 40 ng / mL IFN-γ for 12 h and then stimulated with 100 ng / mL LPS for 15 min. Emodin pretreatment was performed. The contents of ERK, JNK and p38 MARK in HT-29 cells and the content of IL-8 in supernatant of cells were detected by ELISA. Results: The phosphorylation of ERK, JNK and p38 MARK and the secretion of IL-8 in HT-29 cells were significantly increased after IFN-γ and LPS stimulation. Emodin significantly inhibited the phosphorylation of p38 and JNK but not ERK phosphorylation. Emodin significantly reduced the production of IL-8 in HT-29 cells induced by IFN-γ + LPS, and Significant dose-dependent. Conclusion: Emodin can effectively inhibit the phosphorylation of p38 and JNK in HT-29 cells induced by IFN-γ + LPS and significantly reduce the secretion of IL-8.