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Quote : 吴源陶,邹译娴,张春虎,王理槐.菝葜皂苷元对结直肠癌细胞HT-29凋亡和自噬的影响[J].湖南中医药大学学报英文版,2021,41(11):1645-1649.[Click to copy ]
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菝葜皂苷元对结直肠癌细胞HT-29凋亡和自噬的影响
吴源陶,邹译娴,张春虎,王理槐
(湖南中医药大学第一附属医院, 湖南 长沙 410007;中南大学湘雅医院中西医结合科, 湖南 长沙 410008)
摘要:
    目的 探讨菝葜皂苷元(sarsasapogenin,SAR)对人结直肠癌细胞HT-29增殖、凋亡和自噬的影响。方法 将HT-29细胞分为对照组(DMEM培养液)和SAR组(DMEM培养液+DMSO+10、20、30、40、50、60 mg/L SAR溶液);分别采用MTT法、流式细胞术、TUNEL染色及MDC染色检测细胞的增殖、凋亡及自噬的变化情况;用Western blot法检测细胞中Caspase-3、Caspase-9、Beclin-1及LC3B蛋白表达水平。结果 经SAR处理后,HT-29细胞的增殖能力明显降低(P<0.05),凋亡和自噬水平明显增加(P<0.05);与对照组相比,SAR组细胞Caspase-3、Caspase-9、Beclin-1及LC3B蛋白表达水平显著上调(P<0.05)。结论 SAR能够抑制结直肠癌细胞增殖,诱导细胞凋亡和细胞自噬的发生,其机制可能与上调Caspase-3、Caspase-9、Beclin-1及LC3B蛋白表达水平有关。
关键词:  菝葜皂苷元  结肠癌  大肠癌  细胞增殖  细胞凋亡  细胞自噬
DOI:10.3969/j.issn.1674-070X.2021.11.001
Received:December 24, 2020  
基金项目:国家自然科学基金项目(81673951);湖南省卫健委资助项目(C2019092);湖南省教育厅资助项目(13C054)。
Effect of Sarsasapogenin on Apoptosis and Autophagy of Colorectal Cancer Lines HT-29
WU Yuantao,ZOU Yixian,ZHANG Chunhu,WANG Lihuai
(The First Affiliated Hospital of Hunan University of Chines Medicine, Changsha, Hunan 410007, China;Xiangya Hospital, Central South University, Changsha, Hunan 410008, China)
Abstract:
    Objective To investigate the effect of sarsasapogenin (SAR) on the proliferation, apoptosis, and autophagy of human colorectal cancer cell HT-29. Methods HT-29 cells were divided into control group (DMEM medium) and SAR group (DMEM medium + DMSO + 10, 20, 30, 40, 50, 60 mg/L SAR solution). MTT, flow cytometry, TUNEL staining, and MDC staining were used to detect the changes of cell proliferation, apoptosis and autophagy; Western blot method was used to detect the expression levels of Caspase-3, Caspase-9, Beclin-1 and LC3B protein. Results After treatment with SAR, the proliferation ability of HT-29 cells was significantly reduced (P<0.05), and the level of apoptosis and autophagy increased significantly (P<0.05). Compared with the control group, the expression levels of Caspase-3, Caspase-9, Beclin-1 and LC3B protein in SAR group were significantly increased (P<0.05). Conclusion SAR can inhibit the proliferation of colorectal cancer cells, induce apoptosis and autophagy. The mechanism may be related to the up-regulation of Caspase-3, Caspase-9, Beclin-1 and LC3B protein expression levels.
Key words:  sarsasapogenin  colon cancer  colorectal cancer  cell proliferation  apoptosis  autophagy
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