HGF介导DXR诱导肝癌细胞的凋亡作用

HGF-mediated Doxorubicin apoptosis-induced for hepatic carcinoma cell

为了解肝细胞生长因子（HGF）对DXR诱导凋亡效用。方法：肝癌细胞处理分为单用组：DXR、ActinD和HGF。联合组DXR（0．0lug／ml）＋HGF（l0，20，30ng／ml）、DXR＋ActinD＋HGF；生理盐水及牛血清白蛋白对照组。测定MTT值，H-E染色及Hoe－chest33258荧光染色观察细胞形态。结果：24h大剂量DXR引起10％癌细胞凋亡、54％细胞死亡，小剂量者无明显诱导凋亡作用；大剂量ActinD凋亡细胞＜30％。HGF10－50ng／ml无明显诱导凋亡效用。DXR（0．0lug／ml）＋HGF(10，20，30ng/ml）组48h后随HGF剂量加大细胞凋亡数亦增加。依次加入DXR、放线菌素D后对HGF介导的效用有抑制性。结论：合用DXR和HGF能够诱导肝癌细胞凋亡，可能与HGF介导的信号传导有关。

Aim Doxorubicin(DXR) has been shown to induce DNA strands braking tempoarily and recombination gene deletion and rearrangements and mutation tO improve apoptosis we used DXR combined with hepatocyte growth factor(HGF) to hepatic cancer cell line(SMMC-7721).Methods Apoptosis was induced by DXR, Actin D, HGF(10,20, 30ng/ml)+DXR(0.0lμg/ml) and physioiogical salt solution and bovine serum albulmin as control. We observed the morphology of apoptosis by H-E and fluency staining. Results At 24h, 10%apoptosis and 54%dead cell were seen in large dose DXR group. Apoptosis was less than 5% (P<0.05)in small group of DXR and 30% larger dose group of ActinD, respectively. It was found that apoptosis was increased in a dose-depen-dent manner by DXR(0.01μg/ml) + HGF(10,20,30ng/ml) groups after 48h. When DXR and Actin D were added in turn, It inhibited the effect Of HGF on apoptosis. Conchusion The DXR + HGF may induce apoptosis in hepatic carcinoma cell line and might be related to signal transduction for HGF.