目的:探讨从中药木鳖子中提取的单体化合物对羟基桂皮醛(p-hydroxylcinnamaldehyde,PHD)对小鼠黑素瘤B16细胞分化的影响及其可能的作用机制。方法:以10、20、40μmol/L PHD作用B16细胞,设空白对照及福司克林(Forskelin)阳性对照组。磺酰罗丹明(suphrhodamineB,SRB)法检测PHD对B16细胞生长的抑制率,平板克隆集落形成实验检测细胞的克隆形成能力,Giemsa染色观察细胞形态,比色法检测细胞中黑色素含量和酪氨酸酶(tyrosinase,Tyr)活性,划痕愈合实验检测细胞的迁移能力,Western blotting检测Tyr、酪氨酸酶相关蛋白1(tyrosinase protein,Trp1)及MAPK信号转导通路中p-P38、pJNK和p-ERK1/2的表达。结果:PHD对黑素瘤B16细胞具有明显的增殖抑制作用,10、20、40μmol/L PHD作用B16细胞48h后,其增殖抑制率与对照组相比明显增加[(12.78±0.87)%、(37.70±2.28)%、(42.17±4.18)%vs 0,P<0.05],20、40μmol/L PHD组增殖抑制率与Forskelin组相比明显增加[(37.70±2.28)%、(42.17±4.18)%vs(22.00±1.13)%,P<0.05]。40μmol/L PHD处理B16细胞24、48、72 h后,B16细胞呈典型分化形态,黑色素含量及Tyr活性与对照组相比均明显增加[(0.097±0.02)、(0.13±0.04)、(0.15±0.05)vs(0.085±0.003);(1.11±0.31)、(1.43±0.05)、(1.67±0.49)vs(0.64±0.10),P<0.05];细胞集落形成能力和迁移能力都明显降低(均P<0.05)。与空白对照组相比,PHD处理组细胞Tyr和Trp1的表达明显增加(P<0.05),MAPK信号通路中p-P38和p-JNK的表达水平也明显增加(P<0.05),而p-ERK活性差异则无统计学意义(P>0.05)。结论:PHD通过上调MAPK信号通路中p-P38和p-JNK的活性而对小鼠黑素瘤B16细胞产生明显的增殖抑制,并在形态和功能上诱导黑素瘤细胞的分化。 OBJECTIVE: To investigate the effect of p-hydroxylcinnamaldehyde (PHD), a monomer extracted from Momordica charantia L. on the differentiation of mouse melanoma B16 cells and its possible mechanism. Methods: B16 cells were treated with 10, 20 and 40 μmol / L PHD, and blank control group and Forskelin positive control group were established. The inhibitory rate of PHD on the growth of B16 cells was detected by SRB method. The colony formation ability of cells was detected by plate clone colony formation assay. The cell morphology was observed by Giemsa staining. The content of melanin and tyrosine Tyrosinase (Tyr) activity and scratch healing assay were used to detect the migration ability of cells. Western blotting was used to detect the expression of Tyr, tyrosinase protein 1 (Trp1) and p-P38, pJNK and p -ERK1 / 2 expression. Results: PHD had a significant inhibitory effect on proliferation of melanoma B16 cells. After treated with 10, 20 and 40 μmol / L PHD for 48 hours, the proliferation inhibition rate of B16 cells was significantly increased compared with that of the control group [(12.78 ± 0.87)%, ( (37.70 ± 2.28)%, (42.17 ± 4.18)% vs 0, P <0.05]. The proliferation inhibition rates in 20,40μmol / L PHD group were significantly higher than those in Forskelin group [(37.70 ± 2.28)% vs (42.17 ± 4.18) % vs (22.00 ± 1.13)%, P <0.05]. Compared with the control group, B16 cells showed a typical differentiation pattern after treated with 40μmol / L PHD for 24, 48 and 72 hours ([(0.097 ± 0.02), (0.13 ± 0.04) and (0.15 ± 0.05) vs (0.085 ± 0.003), (1.11 ± 0.31), (1.43 ± 0.05), (1.67 ± 0.49) vs (0.64 ± 0.10), P <0.05] .The cell colony forming ability and migration ability were significantly decreased All P <0.05). Compared with the blank control group, the expression of Tyr and Trp1 in PHD treatment group was significantly increased (P <0.05), and the expression of p-P38 and p-JNK in MAPK signaling pathway was significantly increased (P <0.05) ERK activity difference was not statistically significant (P> 0.05). CONCLUSION: PHD can significantly inhibit the proliferation of mouse melanoma B16 cells by up-regulating the activity of p-P38 and p-JNK in MAPK signaling pathway and induce the differentiation of melanoma cells morphologically and functionally.