【摘要】 目的探讨番泻苷B对胃癌细胞生长、凋亡、干样特性以及IL-6/JAK2/STAT3通路的影响。方法通过CCK8法检测胃癌细胞SGC-7901的活力,筛选合适剂量;流式检测细胞凋亡;显微观察干细胞成球;流式分选干细胞CD133⁺;Western blot检测干细胞标志物（OCT4、SOX2）;ELISA检测炎症因子（iNOS、IL-6、IL-4）含量;Western blot检测IL-6/JAK2/STAT3通路相关蛋白（IL-6、p-JAK2、p-STAT3）表达。结果 CCK8检测显示,随番泻苷B浓度的增加,对细胞生长的抑制作用显著（P<0.05）,筛选4个剂量组(0、5、10、20μmol·L^-1)进行后续实验。与0μmol·L^-1剂量组相比,5μmol·L^-1剂量组差异不具有显著性,10、20μmol·L^-1剂量组细胞凋亡率、抗炎因子IL-4含量显著增加（P<0.05）,干细胞成球数量及直径、CD133⁺比例、干细胞标志物（OCT4、SOX2）表达、促炎因子iNOS、IL-6含量显著降低（P<0.05）,IL-6、p-JAK2、p-STAT3表达量显著减少（P<0.05）。结论番泻苷B具有抑制胃癌细胞SGC-7901生长、干样特性、炎症因子水平以及诱导肿瘤细胞凋亡的作用,其机制可能与下调IL-6/JAK2/STAT3信号通路活性有关,从而缓解胃癌的发生发展。更多还原

【Abstract】 This study was designed to investigate the effects of senoside B on the growth, apoptosis, stem-like properties and IL-6/JAK2/STAT3 pathway of gastric cancer cells. The activity of gastric cancer cell SGC-7901 was detected by CCK8 method, while the apoptosis of SGC-7901 was detected by flow cytometry. The pellet formation of stem cells was observed by microscopy; CD133⁺stem cells were sorted by flow cytometry. Western blot was used to detect stem cell markers OCT4 and SOX2, while ELISA for the levels of inflammatory factors iNOS, IL-6, IL-4.Furthermore, Western blot also used to detect the expression of IL-6/JAK2/STAT3 pathway related proteins IL-6, p-JAK2, p-STAT3. CCK8 assay showed that the inhibitory effect of senoside B on SGC-7901 cell growth was significant（P < 0.05）, and 4 dose groups of senoside B(0, 5, 10, 20 μmol·L^-1) were screened out for subsequent experiments. Compared with 0 μmol·L^-1 dose group, 5 μmol·L^-1 dose group has no significant difference, while 10,20 μmol·L^-1 dose groups demonstrated higher level of apoptosis rate and anti-inflammatory factor IL-4（P < 0.05）,lower level of stem cell pellet formation and pellet diameter, as well as lower level of CD133⁺, OCT4, SOX2, iNOS,IL-6, p-JAK2, and p-STAT3（P<0.05）. These results indicated that senoside B could inhibit the growth, the stem-like properties and inflammatory factors levels of gastric cancer cells SGC-7901, and induce the apoptosis of tumor cells. The mechanism may be related to the down-regulation of IL-6/JAK2/STAT3 signaling pathway activity, thus postponing the occurrence and development of gastric cancer.更多还原