Wang Li, Li Yulin, Zhu Lidan, Yin Ran, Wang Ren, Luo Xiaohu, Li Yongfu, Li Yanan, Chen Zhengxing
Key Laboratory of Carbohydrate Chemistry and Biotechnology Ministry of Education, State Key Laboratory of Food Science and Technology, Collaborative Innovation Center for Food safety and quality control, Jiangsu province, National Engineering Laboratory for Cereal Fermentation Technology, School of Food Science and Technology, Jiangnan University, Wuxi, 214122,Jiangsu, China.
Hubei Key Laboratory of Edible Wild Plants Conservation and Utilization, 11 Cihu Road, Huangshi, 435002, China.
Int J Biol Macromol. 2016 Jul;88:424-32. doi: 10.1016/j.ijbiomac.2016.04.016. Epub 2016 Apr 8.
Polysaccharides purified from rice bran show antitumor activity against tumor cells, yet the mechanism of this action remains poorly understood. To address this issue, our study evaluated the effect of rice bran polysaccharides on mouse melanoma cell line B16, and Raw264.7 macrophages. Rice bran polysaccharides (RBP) failed to inhibit B16 cell growth in vitro. However, Raw264.7 macrophages treated by RBP enhancement of cytotoxic effects. The cytotoxicity was confirmed by the stimulation of nitric oxide (NO) production and tumor necrosis factor-α (TNF-α) secretion on Raw264.7 macrophages in a dose-dependent manner. RBP2, a fraction of RBP, notably enhanced the inhibition of B16 cells and boosted the immunepotentiation effect compared with RBP. To further enhance the inhibition of B16 cell growth, sulfated polysaccharides (SRBP) was derived using the chlorosulfonic acid-pyridine method. SRBP2 was found to suppress B16 cell growth, reduce B16 cell survival and stimulate NO and TNF-α production. However, SRBP2 displayed a cytotoxic effect on Raw264.7 macrophages. These results suggest that the antitumor activity of RBP and RBP2 is mediated mainly through the activation of macrophages. SRBP2 exerts its antitumor activity by inducing apoptosis in tumor cells and the secretion of NO and TNF-α.
从米糠中纯化得到的多糖对肿瘤细胞具有抗肿瘤活性，但其作用机制仍知之甚少。为解决这一问题，我们的研究评估了米糠多糖对小鼠黑色素瘤细胞系B16和Raw264.7巨噬细胞的影响。米糠多糖（RBP）在体外未能抑制B16细胞生长。然而，RBP处理的Raw264.7巨噬细胞增强了细胞毒性作用。通过以剂量依赖方式刺激Raw264.7巨噬细胞产生一氧化氮（NO）和分泌肿瘤坏死因子-α（TNF-α），证实了细胞毒性。RBP的一个组分RBP2与RBP相比，显著增强了对B16细胞的抑制作用并增强了免疫增强效果。为进一步增强对B16细胞生长的抑制作用，采用氯磺酸-吡啶法制备了硫酸化多糖（SRBP）。发现SRBP2可抑制B16细胞生长，降低B16细胞存活率，并刺激NO和TNF-α的产生。然而，SRBP2对Raw264.7巨噬细胞显示出细胞毒性作用。这些结果表明，RBP和RBP2的抗肿瘤活性主要通过巨噬细胞的激活来介导。SRBP2通过诱导肿瘤细胞凋亡以及分泌NO和TNF-α发挥其抗肿瘤活性。
