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首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Ethyl Acetate Extract of Asclepias curassavica Induced Apoptosis in Human Cancer Cells via Activating p38 and JNK MAPK Signaling Pathways
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Ethyl Acetate Extract of Asclepias curassavica Induced Apoptosis in Human Cancer Cells via Activating p38 and JNK MAPK Signaling Pathways

机译：醋栗提取物乙酸乙酯提取物通过激活p38和JNK MAPK信号通路诱导人癌细胞凋亡

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Background. Asclepias curassavica L. (Asclepiadaceae), as a traditional medicinal plant, is used as treatment for tumors in traditional Chinese and Indian medical practice. However, its underlying molecular mechanisms remain largely unresolved. The current study investigated its antitumor activity and the underlying molecular mechanisms. Method. Cell viability was detected by a real-time cell analysis system and MTT assay. Antitumor effect of ethyl acetate extract of Asclepias curassavica (EAAC) on NIC-H1975 tumors in vivo was assessed in BALB/c-nuu mouse. Apoptosis was measured using Hoechst33342 staining and Annexin V/PI-staining. Apoptosis-related proteins and MAPK signaling pathways were analyzed based on Western blot assay. Results. EAAC exhibited the highest cytotoxic activity in vitro than other polar parts. Meanwhile, EAAC could inhibit sensitive cell line NIC-H1975 proliferation in a concentration-dependent and time-dependent manner. Furthermore, EAAC had a significant inhibitory effect on NIC-H1975 tumor growth in BALB/c-nuu mouse. NIC-H1975 cells showed obvious apoptosis characteristics after EAAC treatment. Fas, caspase family members caspase 3, caspase 9, and caspase 8 showed dose-dependent induction by EAAC treatment, with increasing PARP cleavage. Additionally, EAAC significantly downregulated antiapoptotic proteins Bcl-2, XIAP, survivin, and Mcl-1 and upregulated proapoptosis proteins Bak, Bax, as well as activation of p38 and JNK MAPK signaling pathways. Moreover, inhibiting p38 and JNK MAPK by pharmacological inhibitors abrogated EAAC-induced apoptosis. Conclusion. Our data indicated that EAAC exerted potent antitumor effect both in vitro and in vivo by triggering the apoptotic pathway.
机译：背景。古老的药用植物Ascurpias curassavica L.（Asclepiadaceae）在中国和印度的传统医学实践中用于治疗肿瘤。但是，其潜在的分子机制仍未解决。目前的研究调查了其抗肿瘤活性及其潜在的分子机制。方法。通过实时细胞分析系统和MTT测定法检测细胞活力。在BALB / c-nu / nu小鼠中评估了蛇毒的乙酸乙酯提取物（EAAC）在体内对NIC-H1975肿瘤的抗肿瘤作用。使用Hoechst33342染色和膜联蛋白V / PI染色测量细胞凋亡。基于蛋白质印迹法分析凋亡相关蛋白和MAPK信号通路。结果。 EAAC在体外表现出最高的细胞毒性活性，高于其他极性部分。同时，EAAC可以浓度依赖性和时间依赖性抑制敏感细胞系NIC-H1975的增殖。此外，EAAC对BALB / c-nu / nu小鼠的NIC-H1975肿瘤生长具有显着的抑制作用。 EAAC处理后，NIC-H1975细胞显示出明显的凋亡特征。 Fas，caspase家族成员caspase 3，caspase 9和caspase 8通过EAAC处理显示出剂量依赖性诱导作用，且PARP裂解增加。此外，EAAC显着下调抗凋亡蛋白Bcl-2，XIAP，survivin和Mcl-1，并上调促凋亡蛋白Bak，Bax以及p38和JNK MAPK信号通路的激活。此外，通过药理抑制剂抑制p38和JNK MAPK可消除EAAC诱导的细胞凋亡。结论。我们的数据表明，EAAC通过触发凋亡途径，在体内和体外均发挥了有效的抗肿瘤作用。

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