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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。
To understand the effect of hepatocyte growth factor (HGF) on DXR-induced apoptosis. Methods: Hepatoma cell lines were divided into single-use groups: DXR, ActinD, and HGF. Combined group DXR (0.0lug/ml) + HGF (10, 20, 30ng/ml), DXR + ActinD + HGF; saline and bovine serum albumin control group. The MTT value, H-E staining and Hoe-chest33258 fluorescence staining were used to observe the cell morphology. RESULTS: Large doses of DXR at 24 h caused apoptosis in 10% of cancer cells and 54% of cell death. Small doses did not significantly induce apoptosis; large doses of ActinD apoptotic cells were <30%. HGF 10-50 ng/ml did not significantly induce apoptosis. In the DXR(0.0lug/ml)+HGF(10,20,30ng/ml) group, the number of apoptotic cells increased with the increase of HGF dose 48 hours later. The sequential addition of DXR and actinomycin D inhibited the HGF-mediated effects. CONCLUSION: The combination of DXR and HGF can induce apoptosis of hepatoma cells, which may be related to HGF-mediated signal transduction.