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目的:探讨唐古特大黄多糖(Rheum tanguticum polysaceharide,RTP)组分1(RTP1)对60γCo射线诱导的肠上皮细胞IEC-6凋亡的保护作用及其可能的机制。方法:采用大鼠空肠上皮细胞(IEC-6细胞株),共分为4组,正常对照组(Normal Control,NC)、辐射对照组(Irradiation Control,IC)以及RTP1低剂量组(10μg/m1)、中剂量组(30μg/m1)和高剂量组(100μg/m1),以6.0 Gy60Coγ射线一次性照射损伤细胞,损伤前用RTP1预处理细胞48 h。采用MTT比色法测定细胞活力,吖啶橙荧光染色及流式细胞仪检测细胞凋亡的发生,Western blot测定Caspase-3酶活性。结果:6.0 Gy60Coγ射线照射可明显降低细胞存活率并诱导细胞凋亡,凋亡率为31.3%,细胞Caspase-3的活性明显升高,RTP1预处理细胞可明显提高细胞存活率,流式细胞仪检测凋亡率(30、100μg/m1)分别降低至24.4%和21.5%,Caspase-3酶活性降低,并呈现一定的剂量依赖性。结论:RTP1可明显抑制60γCo射线诱导的IEC-6细胞凋亡,其细胞保护作用可能与抑制Caspase-3活性相关。
Objective: To investigate the protective effect of RTP1 (RTP1) on the apoptosis of IEC-6 induced by 60γCo in intestinal epithelial cells and its possible mechanism. Methods: The rat jejunal epithelial cells (IEC-6 cell line) were divided into 4 groups: Normal Control (NC), Irradiation Control (IC) and low dose RTP1 (30μg / ml) and high dose group (100μg / ml). The cells were pretreated with 6.0 Gy of 60Co γ ray for 48 h. Cell viability was measured by MTT colorimetric assay. Apoptosis was detected by acridine orange staining and flow cytometry. Caspase-3 activity was detected by Western blot. Results: 6.0 Gy60Coγ-ray irradiation can significantly reduce cell viability and induce apoptosis, the apoptosis rate was 31.3%, the activity of Caspase-3 cells was significantly increased, RTP1 pretreatment cells can significantly improve cell viability, flow cytometry The apoptosis rate (30,100μg / ml) was reduced to 24.4% and 21.5%, respectively. The activity of Caspase-3 was decreased and showed a dose-dependent manner. Conclusion: RTP1 can significantly inhibit the apoptosis of IEC-6 cells induced by 60γCo radiation. The protective effect of RTP1 may be related to the inhibition of Caspase-3 activity.