本文選題：肝細胞生長因子 + 慢性髓細胞性白血病　； 參考：《中國藥學雜志》2017年03期

【摘要】：目的觀察肝細胞生長因子(hepatocyte growth factor,HGF)對經凋亡誘導劑足葉乙苷(etoposide,VP-16)誘導后慢性髓細胞性白血病(CML)K562細胞凋亡的抑制作用,并分析其分子機制。方法采用蘇木素-伊紅(HE)染色、吖啶橙染色(AO)染色對凋亡細胞形態(tài)特征變化進行定性/半定量分析;采用Annexin V-FITC/PI雙染、JC-1染色檢測細胞膜表面的PS外翻和完整性及線粒體膜電位分析凋亡細胞生化特征變化;采用熒光定量聚合酶鏈反應(PCR)檢測Bcl-2、Bax、Caspase-3、Caspase-9等凋亡相關基因mRNA表達的變化,綜合評價HGF抗凋亡效應,并闡述其分子機制。結果 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組早期凋亡細胞明顯低于VP-16組(P0.05、P0.001),提示HGF具有抗K562細胞早期凋亡效應;凋亡相關基因mRNA表達檢測結果發(fā)現(xiàn),HGF+VP-16組的Bcl-2 mRNA表達量明顯高于VP-16組(P0.001),而Bax mRNA、Caspase-3 mRNA、Caspase-9 mRNA表達量明顯低于VP-16組(P0.05、P0.001、P0.001),證實HGF抑制凋亡基因表達,同時促進抗凋亡基因的表達,提示HGF具抗凋亡效應。結論 HGF顯著抑制經VP-16誘導的CML K562細胞的凋亡,該抗凋亡效應可能通過HGF/c-Met途徑調控PI3K/AKT通路而實現(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 浙江省醫(yī)學遺傳學重點實驗室;寧波市泌尿腎病醫(yī)院;
【基金】：浙江省醫(yī)藥衛(wèi)生科技項目(2014KYB243) 寧波市科技計劃( 2014C50015、2013A610244、2013A610219、2010A610031)
【分類號】：R73-36

【相似文獻】

相關期刊論文 前1條

1 姚鵬;胡大榮;;核轉錄因子-κB在肝細胞生長因子介導的肝干細胞抗凋亡效應中的作用[J];實用醫(yī)學雜志;2009年03期

，

本文編號：1796277