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Archive > Volume 10 Issue 4 > 2018,10(4):437-444. DOI:10.1016/j.chmed.2018.08.009 Prev Next

花椒毒素通過死亡受體途徑誘導(dǎo)胃癌SGC-7901細(xì)胞凋亡

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Xanthotoxin induces apoptosis in SGC-7901 cells through death receptor pathway

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    摘要:
    目的 研究傘形科藥用植物花椒毒素對(duì)細(xì)胞增殖和凋亡的影響，并探究其對(duì)人胃癌SGC-7901細(xì)胞的體外作用機(jī)制。 方法 用不同濃度的花椒毒素（10，20，60，80，100，120，140和160μg/ mL）處理SGC-7901，HepG-2，MCF-7和A549細(xì)胞48h，用MTT法測(cè)定細(xì)胞活力（IC 50）；用Hoechst 33258染色試劑盒和Annexin V-FITC凋亡檢測(cè)試劑盒觀察花椒毒素誘導(dǎo)的細(xì)胞凋亡；流式細(xì)胞術(shù)檢測(cè)花椒毒素處理后人胃癌SGC-7901細(xì)胞凋亡相關(guān)蛋白Fas / FasL，Bid和DR5 / TRAIL； 通過Flouormetric Assay Kit測(cè)定花椒毒素對(duì)細(xì)胞中Caspase-8蛋白表達(dá)的影響。 結(jié)果 花椒毒素明顯抑制SGC-7901，HepG-2，MCF-7和A549細(xì)胞增殖，其抑制作用呈濃度依賴性;；流式細(xì)胞術(shù)結(jié)果顯示，在一定濃度范圍內(nèi)，黃嘌呤毒素可以以濃度依賴性方式增加Fas / FasL和DR5 / TRAIL蛋白的表達(dá)水平。 細(xì)胞中Bid蛋白含量增加，且表現(xiàn)出濃度依賴性。 結(jié)論 花椒毒素可通過Fas / FasL蛋白介導(dǎo)的死亡受體途徑或DR5 / TRAIL介導(dǎo)的死亡受體途徑在一定濃度范圍內(nèi)誘導(dǎo)SGC-7901細(xì)胞凋亡，并增加死亡受體蛋白的表達(dá)水平，激活Caspase-8，激活下游影響因子，誘導(dǎo)細(xì)胞凋亡，或激活Caspase-8切割蛋白Bid，然后進(jìn)入線粒體途徑，誘導(dǎo)細(xì)胞凋亡。

    Abstract:
    Objective To investigate the effects of xanthotoxin from Apiaceae medicinal plants on cell proliferation and apoptosis, and explore its mechanism of action against human gastric carcinoma SGC-7901 cells in vitro. Methods SGC-7901, HepG-2, MCF-7, and A549 cells were treated with different concentrations of xanthotoxin (10, 20, 60, 80, 100, 120, 140, and 160 μg/mL) for 48 h, and the cell viability (IC50) was determined by MTT assay; Xanthotoxin-induced apoptosis in cells was observed by using Hoechst 33258 Staining Kit and Annexin V-FITC Apoptosis Detection Kit; Flow cytometry was used to detect apoptosis related proteins of Fas/FasL, Bid, and DR5/TRAIL proteins in human gastric carcinoma SGC-7901 cells after being treated by xanthotoxin; The influence of xanthotoxin on Caspase-8 protein expression in the cells was determined by Flouormetric Assay Kit. Results Xanthotoxin obviously inhibited SGC-7901, HepG-2, MCF-7, and A549 cells proliferation, and its inhibition was in a concentration-dependened manner; Flow cytometry results showed that in a certain concentration range, xanthotoxin can increase the expression levels of Fas/FasL and DR5/TRAIL proteins in a concentration-dependence manner. The content of bid protein in cells was increased, and it showed concentration-dependence. Conclusion Xanthotoxin may induce SGC-7901 cells apoptosis in a certain concentration range through the Fas/FasL protein mediated death receptor pathway, or by DR5/TRAIL mediated death receptor pathway, and increase the expression level of death receptor protein, activation Caspase-8, activating downstream effect factor, inducing cell apoptosis, or activate Caspase-8 cutting activate protein Bid, and then enter the mitochondrial pathway, induction of apoptosis.

    關(guān)鍵詞:
    細(xì)胞凋亡;死亡受體途徑;DR5/ TRAIL;Fas / FasL;;SGC-7901細(xì)胞;花椒毒素

    Keywords:


    Project Supported:
    Harbin University of Commerce Research Funding (17X072)

    Clc Number:

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