甜菜红素恢复HeLa、HepG2和A549细胞线粒体形态完整和促进细胞核坏死的作用

Betanin Induces Nuclear Necrosis and Mitochondria Intact of HeLa, HepG2 and A549 Cells

目的研究甜菜红素对人宫颈上皮癌HeLa细胞、人肝癌HepG2细胞和人肺腺癌A549细胞线粒体和细胞核等超微结构的影响。方法分别将0、62.5和500 ppm甜菜红素加入HeLa、HepG2和A549细胞培养36 h,在8 000~30 000倍透射电子显微镜下,观察细胞核、线粒体等细胞超微结构,并计算线粒体数量和截表面积。结果 HeLa、HepG2和A549肿瘤细胞核具备肿瘤细胞的特征,并且线粒体肿胀、脊膜结构消失。加入62.5 ppm甜菜红素时,HeLa、HepG2和A549细胞的线粒体计数分别增加10.9%、25.0%和12.6%,截表面积较0 ppm浓度组分别减小38.9%、70.1%和65.3%;加入500 ppm甜菜红素时,HeLa、HepG2和A549细胞的线粒体计数分别增加15.2%、79.7%和40.0%,截表面积较0 ppm浓度组分别减小67.8%、77.6%和81.9%;并且线粒体内膜结构趋于完整。加入500 ppm甜菜红素时,以上三种细胞均出现核分裂、固缩和溶解的坏死相。加入甜菜红素时,HeLa和A549细胞出现凋亡小体,HepG2和A549细胞出现自噬体。结论甜菜红素可促进肿瘤细胞线粒体形态结构恢复,引起细胞核坏死和细胞死亡。

Objective To evaluate the effect of betanin on the ultrastructural changes of mitochondria and nuclei of the human cervical carcinoma HeLa cells, human hepatoma HepG2 cells and human lung adenocarcinoma A549 cells. Methods The experiment was performed on three cell lines cultured for 36 h after exposing to betanin at a dose of 0, 62.5 and 500 ppm respectively. The effect of betanin on the mitochondria, nuclear and other parts of the cells was observed under the field of magnified 8 000-30 000 times electron microscope, and the number and cross-sectional area of mitochondria were calculated. Results The normal HeLa, HepG2 and A549 cells showed typical nuclear characteristics of the tumor cells, with the swelling and cristae membrane disappearance of the mitochondria. Compared with betanin（0 ppm） group, the mitochondria number of the HeLa, HepG2 and A549 cells were increased by 10.9%, 25.0% and 12.6% respectively, and the cross-sectional area of mitochondria were reduced by 38.9%、70.1% and 65.3% respectively in betanin（62.5 ppm） group; the mitochondria numbers of the HeLa, HepG2 and A549 cells were increased by 15.2%, 79.7% and 40.0% respectively, while the cross-sectional areas of mitochondria were reduced by 67.8%, 77.6% and 81.9% respectively in betanin（500 ppm） group, moreover, the cristae membrane of the mitochondria was tended to intact. When betanin was added up to 500 ppm, all cells showed a necrotic phenomenon with the nuclear division, condensation and dissolution. After adding the betanin, the apoptotic bodies were found in Hela and A549 cells; and the autophagy appeared in HepG2 and A549 cells. Conclusion Betanin could promote the recovery of the mitochondria morphology and structure of the tumor cells, and induce the nuclear necrosis and cell death.