本文選題：肝細(xì)胞生長(zhǎng)因子 + 慢性髓細(xì)胞性白血病　； 參考：《中國藥學(xué)雜志》2017年03期

【摘要】：目的觀察肝細(xì)胞生長(zhǎng)因子(hepatocyte growth factor,HGF)對(duì)經(jīng)凋亡誘導(dǎo)劑足葉乙苷(etoposide,VP-16)誘導(dǎo)后慢性髓細(xì)胞性白血病(CML)K562細(xì)胞凋亡的抑制作用,并分析其分子機(jī)制。方法采用蘇木素-伊紅(HE)染色、吖啶橙染色(AO)染色對(duì)凋亡細(xì)胞形態(tài)特征變化進(jìn)行定性/半定量分析;采用Annexin V-FITC/PI雙染、JC-1染色檢測(cè)細(xì)胞膜表面的PS外翻和完整性及線粒體膜電位分析凋亡細(xì)胞生化特征變化;采用熒光定量聚合酶鏈反應(yīng)(PCR)檢測(cè)Bcl-2、Bax、Caspase-3、Caspase-9等凋亡相關(guān)基因mRNA表達(dá)的變化,綜合評(píng)價(jià)HGF抗凋亡效應(yīng),并闡述其分子機(jī)制。結(jié)果 HE法、AO法發(fā)現(xiàn)HGF+VP-16組凋亡率明顯低于VP-16組(P0.05、P0.05),提示HGF可顯著抑制凋亡的發(fā)生;Annexin V-FITC/PI雙染法、JC-1染色法發(fā)現(xiàn)HGF+VP-16組早期凋亡細(xì)胞明顯低于VP-16組(P0.05、P0.001),提示HGF具有抗K562細(xì)胞早期凋亡效應(yīng);凋亡相關(guān)基因mRNA表達(dá)檢測(cè)結(jié)果發(fā)現(xiàn),HGF+VP-16組的Bcl-2 mRNA表達(dá)量明顯高于VP-16組(P0.001),而Bax mRNA、Caspase-3 mRNA、Caspase-9 mRNA表達(dá)量明顯低于VP-16組(P0.05、P0.001、P0.001),證實(shí)HGF抑制凋亡基因表達(dá),同時(shí)促進(jìn)抗凋亡基因的表達(dá),提示HGF具抗凋亡效應(yīng)。結(jié)論 HGF顯著抑制經(jīng)VP-16誘導(dǎo)的CML K562細(xì)胞的凋亡,該抗凋亡效應(yīng)可能通過HGF/c-Met途徑調(diào)控PI3K/AKT通路而實(shí)現(xiàn)。
[Abstract]:Objective to observe the inhibitory effect of hepatocyte growth factor (HGF) on the apoptosis of chronic myeloid leukemia (CML) K562 cells induced by etoposideside VP-16, and to analyze its molecular mechanism. Methods the morphological changes of apoptotic cells were qualitatively and semi-quantitatively analyzed by hematoxylin eosin (HE) staining and acridine orange staining (AOO). Annexin V-FITC/PI double staining JC-1 staining was used to detect PS valgus and integrity on cell membrane surface and mitochondrial membrane potential to analyze the biochemical characteristics of apoptotic cells, and fluorescent quantitative polymerase chain reaction (FQ-PCR) was used to detect the changes of mRNA expression of apoptosis-related genes such as Bcl-2Caspase-3Caspase-9. The antiapoptotic effect of HGF was comprehensively evaluated and its molecular mechanism was expounded. Results the apoptosis rate of HGF VP-16 group was significantly lower than that of VP-16 group P0.05 P0.05A, which suggested that HGF could significantly inhibit apoptosis. The results showed that the early apoptotic cells in HGF VP-16 group were significantly lower than that in VP-16 group P0.05 and P0.001, suggesting that HGF had anti-K562 thin cells. Early apoptosis; The expression of Bcl-2 mRNA in HGF VP-16 group was significantly higher than that in VP-16 group, while the expression of Caspase-3 mRNA-caspase-9 mRNA in Bax mRNAs was significantly lower than that in VP-16 group. It was confirmed that HGF inhibited the expression of apoptotic gene and promoted the expression of anti-apoptotic gene. The results suggest that HGF has anti-apoptosis effect. Conclusion HGF significantly inhibits the apoptosis of CML K562 cells induced by VP-16, and the anti-apoptotic effect may be achieved through the regulation of PI3K/AKT pathway by HGF/c-Met pathway.
【作者單位】： 寧波市第一醫(yī)院;溫州醫(yī)科大學(xué) 浙江省醫(yī)學(xué)遺傳學(xué)重點(diǎn)實(shí)驗(yàn)室;寧波市泌尿腎病醫(yī)院;
【基金】：浙江省醫(yī)藥衛(wèi)生科技項(xiàng)目(2014KYB243) 寧波市科技計(jì)劃( 2014C50015、2013A610244、2013A610219、2010A610031)
【分類號(hào)】：R73-36

【相似文獻(xiàn)】

相關(guān)期刊論文 前1條

1 姚鵬;胡大榮;;核轉(zhuǎn)錄因子-κB在肝細(xì)胞生長(zhǎng)因子介導(dǎo)的肝干細(xì)胞抗凋亡效應(yīng)中的作用[J];實(shí)用醫(yī)學(xué)雜志;2009年03期

，

本文編號(hào)：1796277