朱彤,贺俊博,武欣,等.东南景天提取物减缓人小肠上皮细胞HIEC-6辐射损伤机制的初步研究[J].中华放射医学与防护杂志,2022,42(7):493-498.Zhu Tong,He Junbo,Wu Xin,et al.Mechanism of Sedum alfredii extract alleviating radiation damage in human small intestinal epithelial cells HIEC-6[J].Chin J Radiol Med Prot,2022,42(7):493-498 |
东南景天提取物减缓人小肠上皮细胞HIEC-6辐射损伤机制的初步研究 |
Mechanism of Sedum alfredii extract alleviating radiation damage in human small intestinal epithelial cells HIEC-6 |
投稿时间:2022-01-04 |
DOI:10.3760/cma.j.cn112271-20220104-00002 |
中文关键词: 东南景天提取物 电离辐射损伤 PRKN 内质网 活性氧 |
英文关键词:Sedum alfredi extract Radiation damage PRKN Endoplasmic reticulum ROS |
基金项目:国家自然科学基金(81730086);中国医学科学院医学与健康科技创新工程项目(2021-I2M-1-042);中央高校基本科研业务费专项资金(3332019098) |
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中文摘要: |
目的 初步确定东南景天提取物(SafE)缓解人小肠上皮细胞HIEC-6辐射损伤的机制。方法 将HIEC-6细胞分为对照组(Con)、照射组(IR)、单独提取物组(SafE)、提取物照射组(SafE+IR)。SafE组使用0.02 g/ml(W/V)SafE处理24 h后,给予2、4、6 Gy γ射线照射,照后24 h检测细胞活力(CCK-8法)和细胞内活性氧(ROS)水平;4 Gy照后24 h取样进行转录组分析,检测细胞内E3泛素连接酶PRKN表达水平,使用荧光染料观察内质网,并统计内质网厚度。结果 与IR组相比,SafE+IR组照射后细胞活力值显著增加(t=2.94~10.40,P<0.05); 与对照组相比,SafE+IR组照射后胞内ROS水平显著降低(t=-13.29~-4.53, P<0.05)。初步筛选出SafE靶基因为PRKN;SafE可维持照射后PRKN转录水平和内质网厚度,IR组与对照组比较,差异有统计学意义(t=-5.55、3.27,P<0.05);SafE组与SafE+IR组比较,差异无统计学意义(P>0.05)。结论 SafE可有效维持内质网厚度,减少细胞辐射损伤,其靶基因 PRKN受电离辐射调控。 |
英文摘要: |
Objective To confirm the mechanism of Sedum alfredii extract (SafE) alleviating radiation injury in human small intestinal epithelial cells (HIEC-6). Methods HIEC-6 cells were divided into 4 groups, including control group (Con), irradiation group (IR), SafE alone group (SafE) and SafE plus irradiation group (SafE+IR). All of the SafE groups were treated with 0.02 g/ml (W/V) SafE for 24 h. Cell viability (CCK-8 method ) and intracellular ROS levels were investigated at 24 h after 2, 4, and 6 Gy irradiation. Samples were taken at 24 h after 4 Gy irradiation for transcriptome analysis, and the intracellular E3 ubiquitin ligase PRKN expression level was measured. The thickness of endoplasmic reticulum was detected at 24 h after 4 Gy irradiation using fluorescent dye. Results SafE could maintain cell viability after irradiation (t=2.94-10.40, P<0.05), and significantly reduced the level of ROS in the irradiated cells (t=-13.29--4.53, P<0.05). PRKN was preliminarily verified to be the target gene of SafE that maintained PRKN transcript level and endoplasmic reticulum thickness after irradiation (IR group vs. Con group: t=-5.55, 3.27, P<0.05, SafE group vs. SafE+IR group: P>0.05).Conclusion SafE is effective in maintaining ER thickness and reducing cellular radiation damage and its target gene PRKN could be regulated by ionizing radiation. |
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