Effect of Korean Red Ginseng Extract on Cell Death Responses in Peroxynitrite-Treated Keratinocytes
Effect of Korean Red Ginseng Extract on Cell Death Responses in Peroxynitrite-Treated Keratinocytes
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DOI：
10.5142/jgr.2010.34.3.205
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发表时间：
2010-09-01
影响因子：
6.3
通讯作者：
Park, Jong Kun
中科院分区：
文献类型：
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作者：
Do Kim, Hyoung;Ha, Se Eun;Park, Jong Kun
韩国红参（KRG）已在世界范围内被用作治疗各种疾病的传统药物，包括癌症。在这项研究中，我们确定了KRG对HaCaT细胞对过氧亚硝酸盐（ONOO-）的反应的影响。在与对照培养基一起孵育12小时之前用ONOO-（2 mM）处理的细胞显示出降低的活力，如使用3[4，5-二甲基噻唑-2-基]-2，5-二苯基四唑溴化物测定所测定的（活力约为未处理的对照细胞的活力的48%）。当KRG被添加到培养后的培养基中时，ONOO-对细胞活力的负面影响显著降低。逆转录聚合酶链反应分析表明，KRG单独没有显着改变p53或“生长停滞和DNA损伤”（GADD）45 mRNA水平。然而，在ONOO处理的细胞中，在孵育后培养基中加入KRG显著且剂量依赖性地降低了p53和GADD 45 mRNA的水平。Western印迹分析显示，与对照培养基孵育的细胞相比，与KRG孵育降低了ONOO处理的细胞中p53和GADD 45蛋白水平。总的来说，这些结果表明，韩国红参提取物保护细胞对ONOO-诱导的遗传毒性，通过调节p53信号传导中间体的表达，增加细胞活力。
Korean red ginseng (KRG) has been used worldwide as a traditional medicine for the treatment of various diseases, including cancer. In this study, we determined the effect of KRG on the responses of HaCaT cells to peroxynitrite (ONOO-). Cells treated with ONOO- (2 mM) prior to incubation with control medium for 12 hours displayed reduced viability, as determined using the 3[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay (viability about 48% of that of non-treated control cells). When KRG was added to the post-incubation medium, the negative effects of ONOO- on cell viability were significantly reduced. Reverse transcription-polymerase chain reaction analysis indicated that KRG alone did not significantly alter p53 or "growth arrest and DNA damage" (GADD)45 mRNA levels. However, the addition of KRG to the post-incubation medium significantly and dose-dependently reduced levels of p53 and GADD45 mRNA in ONOO--treated cells. Western blot analyses revealed that incubation with KRG decreased p53 and GADD45 protein levels in ONOO--treated cells, relative to those in cells incubated with control medium. Collectively, these results suggest that Korean red ginseng extract protects cells against ONOO--induced genotoxicity by increasing cell viability through modulating the expression of p53 signaling intermediates.