Ginsenoside Rh2 and Rg3 inhibit cell proliferation and induce apoptosis by increasing mitochondrial reactive oxygen species in human leukemia Jurkat cells.
Ginsenoside Rh2 and Rg3 inhibit cell proliferation and induce apoptosis by increasing mitochondrial reactive oxygen species in human leukemia Jurkat cells.
复制标题
人参皂苷 Rh2 和 Rg3 通过增加人白血病 Jurkat 细胞线粒体活性氧来抑制细胞增殖并诱导细胞凋亡
DOI：
10.3892/mmr.2017.6459
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发表时间：
2017-06
影响因子：
3.4
通讯作者：
Fang JP
中科院分区：
文献类型：
--
作者：
Xia T;Wang YN;Zhou CX;Wu LM;Liu Y;Zeng QH;Zhang XL;Yao JH;Wang M;Fang JP
人参皂苷Rh 2（Ginsenoside Rh 2，GRh 2）和人参皂苷Rg 3（Ginsenoside Rg 3，GRg 3）是人参中的主要活性成分。本研究旨在探讨GRh 2和GRg 3诱导人白血病Jurkat细胞凋亡的机制。细胞计数试剂盒-8测定用于测定细胞增殖。Hoechst 33342染色、Annexin V-别藻蓝蛋白和7-氨基-放线菌素D法检测细胞凋亡。使用线粒体活性氧（ROS）清除剂mitoTEMPO来检测线粒体ROS对细胞活力和线粒体膜电位（MMP）的影响。最后，通过蛋白质印迹分析评估了许多与神经细胞凋亡相关的蛋白质的表达水平。这些结果表明，GRh 2和GRg 3抑制细胞生长和诱导凋亡，并且GRh 2比GRg 3具有更大的细胞毒性。在Jurkat细胞中，与GRg 3相比，GRh 2诱导产生更多的线粒体ROS;然而，这种效果通过随后用mitoTEMPO处理而得到改善。此外，GRh 2诱导的过量线粒体ROS在抑制细胞增殖和降低MMP方面比GRg 3更有效。此外，与GRg 3相比，GRh 2处理的Jurkat细胞中凋亡相关蛋白的表达水平显著增加。总之，这些研究结果表明，GRh 2和GRg 3通过增加人白血病Jurkat细胞中的线粒体ROS诱导细胞相关凋亡。GRh 2可能比GRg 3更有效地抑制细胞生长和促进细胞凋亡。本研究为急性淋巴细胞白血病的治疗提供了一种潜在的新策略。
Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are primary bioactive components in Panax ginseng. The present study aimed to investigate the underlying mechanisms of apoptotic cell-death induced by GRh2 and GRg3 in human leukemia Jurkat cells. The Cell Counting kit-8 assay was used to determine cell proliferation. Apoptosis was detected by nuclear morphologic observation by Hoechst 33342 staining and Annexin V-allophycocyanin and 7-amino-actinomycin D assay. mitoTEMPO, a mitochondrial reactive oxygen species (ROS) scavenger, was used to examine the effects of mitochondrial ROS on cell viability and mitochondrial membrane potential (MMP). Finally, the expression levels of numerous mitochondrial-associated apoptosis proteins were assessed by western blot analysis. These results demonstrated that GRh2 and GRg3 inhibited cell growth and induced apoptosis, and that GRh2 had greater cytotoxicity than GRg3. GRh2 induced generation of more mitochondrial ROS compared with GRg3 in Jurkat cells; however, this effect was ameliorated by subsequent treatment with mitoTEMPO. Furthermore, excess mitochondrial ROS induced by GRh2 was more potent than GRg3 in inhibiting cell proliferation and reducing MMP. In addition, expression levels of apoptosis-associated proteins were significantly increased in Jurkat cells treated with GRh2 than GRg3. In conclusion, these findings suggested that GRh2 and GRg3 induce mitochondrial-associated apoptosis by increasing mitochondrial ROS in human leukemia Jurkat cells. GRh2 may more effectively inhibit cell growth and accelerate apoptosis than GRg3. This study provides a potential novel strategy for the treatment of acute lymphoblastic leukemia.