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Inhibition of diammonium glycyrrhizinate on mitomycin C-induced apoptosis in HepG2 cells via apoptotic pathway
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摘要: 目的探讨18α-甘草酸二铵对丝裂霉素（MMC）诱导的HepG2细胞凋亡的影响及机制。方法 18α-甘草酸二铵不同浓度与低剂量MMC（50μg/ml）MMC联合作用,采用MTT比色法观察MMC对HepG2细胞活性率的影响;流式细胞术分析凋亡细胞的百分率、线粒体膜电位的改变及Caspase-3的活性变化;Western Blot检测细胞内细胞色素C的表达及凋亡相关蛋白Bcl-2/Bax的表达情况。结果单独MMC（50μg/ml）处理的HepG2细胞活性率明显降低,凋亡率显著增加,线粒体膜电位下降,Caspase-3活性增加,细胞内细胞色素C表达增加,抗凋亡蛋白Bcl-2表达减少,而促凋亡蛋白Bax表达增加。不同浓度的18α-甘草酸二铵与MMC合用组,这些指标的变化均受到抑制。结论 18α-甘草酸二铵可抑制MMC诱导的HepG2细胞凋亡,其机制可能通过调控凋亡相关蛋白的表达而实现。Abstract: Objective To study the inhibition of diammonium glycyrrhizinate on mitomycin C-induced apoptosis in HepG2 cells via apoptotic pathway.Methods Low dose MMC (50 μg/ml) was used to induce the apoptosis of HepG2 cells.Dose-independent inhibition effect of diammonium glycyrrhizinate on MMC-induced apoptosis was determined.MTT method was used to detect the cell survival rates.Flow cytometry was applied to assess cell apoptosis, mitochondrial membrane permeability and Caspase-3 activity.Western Blot was used to check the expression of apoptosis-related proteins cytochrome C, Bcl-2 and Bax.Results The viability of HepG2 cells decreased significantly after being treated with low dose (50 μg/ml) MMC and apoptosis of HepG2 cells was induced, which might be the outcome of up-regulated expression of pro-apoptotic Bax protein and cytochrome C, down-regulated expression of anti-apoptotic Bcl-2, subsequent Caspase-3 activation and loss of mitochondrial transmembrane potential.But these changes were obviously inhibited by diammonium glycyrrhizinate.Conclusion Diammonium glycyrrhizinate can inhibit MMC-induced HepG2 cell apoptosis via regulation of apoptotic pathway.
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Key words:
- mitomycin /
- glycyrrhetinic acid /
- apoptosis /
- liver neoplasms /
- tumor cells
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[1]Pritsos CA, Briggs LA, Gustafson DL.A new cellular target formitomycin C:a case for mitochondrial DNA[J].Oncol Res, 1997, 9 (6-7) :333-337. [2]Pirnia F, Schneider E, Betticher DC, et al.Mitomycin C inducesapoptosis and caspase-8 and-9 processing through acaspase-3 and Fas-independent pathway[J].Cell Death Differ, 2002, 9 (9) :905-914. [3]刘希奎, 周洪美, 张银华.甘利欣在肝动脉栓塞化疗时保肝作用的临床观察[J].中国综合临床, 2002, 18 (11) :1003. [4]和振坤.肝动脉栓塞化疗患者甘草甜素的保肝作用[J].第四军医大学学报, 2004, 25 (18) :1677-1678. [5]Dias N, Bailly C.Drugs targeting mitochondrial functions to controltumor cell growth[J].Biochem Pharmacol, 2005, 70 (1) :1-12. [6]Mignotte B, Vayssiere JL.Mitochondria and apoptosis[J].Eur JBiochem, 1998, 252 (1) :1-15. [7]王海燕, 王来栓, 归绥琪.细胞凋亡通路研究进展[J].国外医学:生理病理科学与临床分册, 2003, 23 (5) :490-492. [8]李龙辉, 左国庆, 汤为学.甘利欣对体外诱导的酒精性脂肪肝细胞的影响[J].重庆医学, 2006, 35 (2) :128-130. [9]Rupniewska Z, Bojarska-Junak A.Apoptosis:mitochondrialmembrane permeabilization and the role played by Bcl-2 familyproteins[J].Postepy Hig Med Dosw (Online) , 2004, 58:538-547. [10]Marzo I, Naval J.Bcl-2 family members as molecular targets incancer therapy[J].Biochem Pharmacol, 2008, 76 (8) :939-946. [11]Kuwana T, Newmeyer DD.Bcl-2-family proteins and the role ofmitochondria in apoptosis[J].Curr Opin Cell Biol, 2003, 15 (6) :691-699. [12]Tsujimoto Y.Role of Bcl-2 family proteins in apoptosis:apoptosomes or mitochondria?[J].Genes Cells, 1998, 3 (11) :697-707. -
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