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首页> 外文期刊>World Journal of Gastroenterology >Induction of apoptosis of human gastric carcinoma SGC-7901 cell line by 5, 7-dihydroxy-8-nitrochrysin in vitro
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Induction of apoptosis of human gastric carcinoma SGC-7901 cell line by 5, 7-dihydroxy-8-nitrochrysin in vitro

机译：5，7-二羟基-8-硝基水杨酸体外诱导人胃癌SGC-7901细胞凋亡

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AIM: To investigate the effect of 5, 7-dihydroxy-8-nitrochrysin (NOChR) on apoptosis of human gastric carcinoma SGC-7901 cell line. METHODS: SGC-7901 cells were cultured in vitro and the inhibitory effect of NOChR on proliferation of SGC-7901 cells was measured by using an MTT assay. NOChR-induced apoptosis rate of SGC-7901 cells was detected using flow cytometry (FCM) with PI staining. DNA ladder bands were observed by DNA agarose gel electrophoresis. The influence of NOChR on the xproxisome proliferator-activated receptor-γ (PPARγ), Bcl-2 and Bax protein expression of SGC-7901 cells was analyzed by Western blot. RESULTS: MTT assay showed that NOChR markedly inhibited proliferation of SGC-7901 cells in a dose-dependent manner, and when IC_(50) was 4.14 μmol/L, the potency of NOChR was 10 times than that of lead compound, chrysin (ChR, IC_(50) was 40.56 μmol/L), and was similar to 5-fluorouracil (5-FU, IC_(50) was 4.51 μmol/L). FCM with propidium iodide (PI) staining demonstrated that the apoptosis rates of SGC-7901 cells treated with 1.25, 5.00 and 20.00 μmol/L NOChR for 48 h were 9.8% ± 0.2%, 36.8% ± 1.9% and 45.5% ± 3.5%, respectively, and were significantly higher when treated with 5.00 and 20.00 μmol/L NOChR than that with 20.00 μmol/L ChR (12.9% ± 1.5%). DNA agarose gel electrophoresis showed that treatment of SGC-7901 cells with 20.00 μmol/L NOChR for 48 h resulted in typical DNA ladder bands of DNA of SGC-7901 cells, which could be eliminated by treating with 10.00 μmol/L GW9662, a blocker of PPARγ. Western blot analysis revealed that after 24 h of treatment with 20.00 μmol/L NOChR, PPARgamma and Bax protein expression of SGC-7901 cells increased but Bcl-2 expression decreased; however, pre-incubation with 10.00 μmol/L GW9662 could efficiently antagonize and weaken the regulatory effect of 20.00 μmol/L NOChR on Bax and Bcl-2 protein expression of SGC-7901 cells. CONCLUSION: NOChR induces apoptosis of SGC-7901 cell lines by activating PPARγ and decreasing ratio of Bcl-2 to Bax.
机译：目的：探讨5，7-二羟基-8-硝基代菊花链（NOChR）对人胃癌SGC-7901细胞凋亡的影响。方法：体外培养SGC-7901细胞，MTT法检测NOChR对SGC-7901细胞增殖的抑制作用。使用PI染色的流式细胞仪（FCM）检测NOChR诱导的SGC-7901细胞凋亡率。通过DNA琼脂糖凝胶电泳观察到DNA梯带。用蛋白质印迹法分析了NOChR对SGC-7901细胞中xproxisome增殖激活受体γ（PPARγ），Bcl-2和Bax蛋白表达的影响。结果：MTT法检测到NOChR明显抑制SGC-7901细胞的增殖，其IC_（50）为4.14μmol/ L时，NOChR的效价为铅化合物chrysin（ChR）的10倍。 ，IC_（50）为40.56μmol/ L），与5-氟尿嘧啶（5-FU，IC_（50）为4.51μmol/ L）相似。 FCM碘化丙啶（PI）染色表明，1.25、5.00和20.00μmol/ L NOChR处理48小时的SGC-7901细胞的凋亡率分别为9.8％±0.2％，36.8％±1.9％和45.5％±3.5％分别为5.00和20.00μmol/ L NOChR处理时，显着高于20.00μmol/ L ChR处理（12.9％±1.5％）。 DNA琼脂糖凝胶电泳显示，用20.00μmol/ L NOChR处理SGC-7901细胞48小时会产生SGC-7901细胞DNA的典型DNA梯带，可通过使用10.00μmol/ L GW9662阻断剂来消除PPARγ。 Western blot分析显示，用20.00μmol/ L的NOChR处理24小时后，SGC-7901细胞的PPARγ和Bax蛋白表达增加，而Bcl-2表达减少。然而，用10.00μmol/ L GW9662预孵育可以有效拮抗并减弱20.00μmol/ L NOChR对SGC-7901细胞Bax和Bcl-2蛋白表达的调节作用。结论：NOChR通过激活PPARγ和降低Bcl-2与Bax的比例诱导SGC-7901细胞凋亡。

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