摘要
[目的]探索黄精多糖对放射性治疗后导致的小肠上皮细胞损伤的影响。[方法]将小肠上皮细胞IEC-6细胞株随机分为4组(2×10^(5)个/组):对照组(正常培养)、放射损伤组(10Gy剂量辐射处理,辐射速度300 cGy/min)、黄精多糖组(10Gy剂量辐射处理,辐射速度300 cGy/min,并加入5 mmol/L黄精多糖处理)、740Y-P组(10Gy剂量辐射处理,辐射速度300 cGy/min,并加入20μmol/L 740Y-P处理),持续处理24 h。通过Brd U实验检测IEC-6细胞增殖水平,流式细胞术分析各组IEC-6细胞凋亡情况,酶联免疫吸附测定法分析各组IEC-6细胞培养基中炎症因子水平,蛋白免疫印迹分析各组IEC-6细胞中PI3K/AKT通路蛋白表达水平。[结果]与放射损伤组比较,黄精多糖组、740Y-P组的IEC-6细胞的增殖率增加(P<0.05),凋亡率下降(P<0.05),炎症因子分泌降低,AKT和PI3K蛋白表达表达降低(P<0.05)。[结论]黄精多糖能通过激活PI3K/AKT信号通路进而促进放射损伤后的IEC-6细胞增殖,减少IEC-6细胞凋亡,抑制炎症因子释放。
[Objective]To investigate the effect of polygona-polysaccharose on radiation-induced injury of small intestinal epithelial cells.[Method]The intestinal epithelial cells(IEC-6 cell line)were randomly divided into 4 groups(2×10^(5)cells/group):the control group(cultured under normal conditions),the radiation injury group(treated with a radiation dose of 10Gy at a speed of 300 cGy/min),the Polygonatum cyrtonema polysaccharide group(treated with a radiation dose of 10Gy at a speed of 300 cGy/min and then treated with 5 mmol/L Polygonatum cyrtonema polysaccharide),and the 740Y-P group(treated with a radiation dose of 10Gy at a speed of 300 cGy/min and then treated with 20µmol/L 740Y-P).The treatment lasted for 24h.The proliferation of IEC-6 cells was detected by BrdU assay,the apoptosis of IEC-6 cells was analyzed by flow cytometry,the levels of inflammatory factors in the culture medium of IEC-6 cells were analyzed by enzyme-linked immunosorbent assay,the protein expression levels of PI3K/AKT pathway in IEC 6 cells of each group were analyzed by Western blot.[Result]Compared with the radiation injury group,the proliferation rate of IEC 6 cells was significantly increased(P<0.05),the apoptosis rate was decreased(P<0.05),the secretion of inflammatory factors was decreased,and the expression of AKT and PI3K protein was decreased in the polygona-polysaccharose and 740Y-P groups(P<0.05).[Conclusion]Polygona-polysaccharose can promote the proliferation of IEC-6 cells after radiation injury by activating PI3K/AKT signaling pathway,reduce the apoptosis of IEC-6 cells,and inhibit the release of inflammatory factors.
作者
刘欢
陈金锁
刘艳莉
宋哲伦
李黎
邢兰花
滕菲
LIU Huan;CHEN Jinsuo;LIU Yanli;SONG Zhelun;LI Li;XING Lanhua;TENG Fei(Department of Radiotherapy,The First Central Hospital of Baoding,Baoding 071000;Department of Urology,Affiliated Hospital of Hebei University,Baoding 071000;Department of Radiotherapy,Affiliated Hospital of Hebei University,Baoding 071000;Department of Critical Care Medicine,The First Central Hospital of Baoding,Baoding 071000,China)
出处
《生物技术》
2025年第6期781-786,共6页
Biotechnology
基金
保定市科技计划项目(2341ZF137)。
关键词
黄精多糖
PI3K
AKT
小肠上皮细胞
放疗
增殖
炎症
凋亡
polygona-polysaccharose
PI3K
AKT
small intestinal epithelial cells
radiotherapy
proliferation
inflammation
apoptosis
