调查ROS/MAPK信号通路在介导香柚苷抑制肝细胞癌SMMC-7721细胞增殖和迁移中的作用。将SMMC-7721细胞用不同浓度的香柚苷处理24小时，并用CCK-8法检测细胞活力的变化。用Transwell和划痕愈合实验评估处理后细胞的迁移和浸润能力，用克隆形成实验评估细胞增殖，用DAPI染色观察细胞核形态的变化。进行Western blotting检测E-cadherin、N-cadherin、MMP-2、MMP-9、PARP、Pro-caspase 3、pJNK、p-P38和p-ERK的表达变化。用Western blotting检测香柚苷对SMMC-7721细胞预处理了ERK、JNK和P38抑制剂（分别为U0126、SB203580和SP600125）后PARP裂解的影响。用DCFH-DA荧光探针检测单独和联合处理N-乙酰半胱氨酸（NAC，30μmol/L）和香柚苷（100、200和300μg/mL）对细胞中反应性氧（ROS）水平的影响。 香柚苷低于50μg/mL对SMMC-7721细胞的活性没有显著影响（P>0.05）。香柚苷的处理显著抑制了细胞划痕愈合、迁移和克隆形成（P＜0.01），减少了N-连接蛋白、MMP-2和MMP-9的蛋白表达（P＜0.01），并上调了E-cadherin的蛋白表达（P＜0.05）。香柚苷处理的SMMC-7721细胞表现出明显的凋亡形态，Procaspase 3的表达降低，PARP的裂解增加（P＜0.01），且JNK、P38和ERK的磷酸化水平增加（P＜0.01）；香柚苷诱导的PARP裂解被U0126和SB203580明显增强，但被SP600125减弱。用300μg/mL香柚苷处理30分钟显著增加了细胞中的ROS水平，这种效应显著被NAC抑制。香柚苷能通过促进ROS产生和激活MAPK信号通路抑制肝细胞癌SMMC-7721细胞的增殖和迁移，并促进凋亡。

To investigate the role of the ROS/MAPK signaling axis in mediating the inhibitory effect of eriocitrin on proliferation and migration of hepatocellular carcinoma SMMC-7721 cells.SMMC-7721 cells were treated with different concentrations of eriocitrin for 24 h, and the changes in cell viability were detected with CCK-8 assay. The migration and invasion abilities of the treated cells were evaluated using Transwell and scratch healing assays, the cell proliferation was assessed with colony-forming assay, and changes in nuclear morphology were observed with DAPI staining. Western blotting was performed to examine the changes in the expressions of E-cadherin, N-cadherin, MMP-2, MMP-9, PARP, Pro-caspase 3, pJNK, p-P38, and p-ERK. The effect of eriocitrin on PARP cleavage in SMMC-7721 cells pretreated with ERK, JNK and P38 inhibitors (U0126, SB203580 and SP600125, respectively) was detected using Western blotting. The effect of treatment with Nacetyl-cysteine (NAC, 30 μmol/L) and eriocitrin (100, 200, and 300 μg/mL), alone or in combination, on reactive oxygen species (ROS) levels in the cells was examined using a DCFH-DA fluorescent probe.Eriocitrin below 50 μg/mL did not produce significant effect on the viability of SMMC-7721 cells (P>0.05). Treatment with eriocitrin significantly inhibited scratch healing, migration, and colony formation of the cells (P < 0.01), reduced the protein expressions of N-cadherin, MMP-2, and MMP-9 (P < 0.01), and up-regulated E-cadherin protein expression (P < 0.05). Eriocitrin-treated SMMC-7721 cells showed obvious apoptotic morphologies with decreased Procaspase 3 expression and increased PARP cleavage (P < 0.01) and phosphorylation levels of JNK, P38, and ERK (P < 0.01); Eriocitrin-induced PAPR cleavage was obviously enhanced by U0126 and SB203580 but attenuated by SP600125. Treatment with 300 μg/mL eriocitrin for 30 min significantly increased ROS level in the cells, and this effect was obviously suppressed by NAC.Eriocitrin can suppress the proliferation and migration and promote apoptosis of hepatocellular carcinoma SMMC-7721 cells by promoting ROS production and activating the MAPKs signaling pathway.