[关键词]
[摘要]
和厚朴酚及厚朴酚是疏水性联苯酚类结构的同分异构体。和厚朴酚能防治结直肠癌CT26细胞或RKO细胞移植瘤在小鼠体内生长,并延长荷瘤小鼠的生存时间。体外实验发现和厚朴酚及厚朴酚能浓度相关地抑制结直肠癌SW480细胞、SW620细胞、LoVo细胞、LS180细胞、CT26细胞、RKO细胞、Caco-2细胞、COLO-205细胞、HCT-8细胞、HCT15细胞、HCT116细胞增殖,并诱导细胞凋亡。在HCT116细胞中,hMLH1错配修复缺失型细胞对和厚朴酚的敏感性高于完整型细胞。和厚朴酚是通过调控JNK/Nur77/AMPK、TGF-β1/p38MAPK/Hippo、BMP7/TGF-β1/p53和BMP7/PTEN/AKT 4条信号转导通路诱导结直肠癌细胞凋亡,还通过抑制血管内皮生长因子的表达,阻滞肿瘤内新生血管形成,抑制结直肠癌生长。和厚朴酚及厚朴酚还能抑制胃癌MGC-803细胞和SGC-7901细胞的增殖。
[Key word]
[Abstract]
Honokiol and magnolol are hydrophobic isomer of biphenol-type structure. Honokiol has the effects in the prophylaxis and treatment for growth of transplantation tumor of colorectal cancer CT26 cells or RKO cells in mice and prolong survival time in mice with bearing tumor. Honokiol and magnolol inhibit proliferation and induce apoptosis in association with dosage on colorectal cancer SW480 cells, SW620 cells, LoVo cells, LS180 cells, TC26 cells, RKO cells, Caco-2 cells, COLO-205 cells, HCT-9 cells, HCT15 cells, and HCT116 cells in vitro. In HCT116 cells, sensibility of hMLH1 mismatch repair defective HCT116 cells to honokiol is higher than hMLH1 mismatch repair proficient HCT116 cells. Honokiol induces colorectal cancer cells apoptosis by regulating four signaling pathways of JNK/Nur77/AMPK, TGF-β1/p38MAPK/Hippo, BMP7/TGF-β1/p53, and BMP7/PTEN/AKT. Honokiol inhibits too growth of colorectal cancer cells by down-regulating the expression of VEGF and decreasing tumor angiogenesis. Honokiol and magnolol inhibit proliferation of gastric carcinoma MGC-803 cells and SGC-7901 cells.
[中图分类号]
R287.5
[基金项目]