Cho Hyung Taek, Kim Jun Ho, Heo Wan, Lee Hyun-Sun, Lee Jeong Jun, Park Tae-Sik, Lee Jin Hyup, Kim Young Jun
1 Department of Food and Biotechnology, Korea University, Sejong-si, Korea.
2 Department of Food Science and Biotechnology, Andong National University, Gyeongsangbuk-do, Korea.
J Med Food. 2019 May;22(5):490-498. doi: 10.1089/jmf.2018.4293.
Although radiation therapy (RT) is a feasible treatment approach for early colorectal cancer, RT is considerably toxic to normal tissues due to the increased reactive oxygen species production, which can induce tissue damage. Ginseng, a natural antioxidant agent, exhibits the protective effects against ionizing radiation (IR)-induced damage in and models. The explosive puffing of ginseng has been investigated as a process to improve the efficacy of ginseng due to the resulting physicochemical changes in its functional components. In this study, we provided the evidence for promotion in the beneficial role of puffed ginseng extract (PGE) and associated mechanisms of action, in comparison with white ginseng extract (WGE), against IR-induced colorectal injury, using study on a mouse model. To study the role of PGE in preventing IR-induced damage, we examined colorectal injury and apoptotic changes in mice exposed to Cs at 8 Gy. High-performance liquid chromatography analysis showed that PGE had an increased total ginsenoside concentration with new generation of Rg3, Rg5, and Rk1, compared with the concentrations in WGE. Administering PGE, but not WGE, significantly ameliorated IR-induced colorectal cell death through negative regulation of apoptotic signaling pathways. These antiapoptotic effects of PGE were linked to the capacity to suppress the p53-mediated DNA damage response and NF-B-mediated apoptotic signaling. Moreover, IR-induced oxidative stress in the colorectal epithelium was markedly reduced by PGE administration. Collectively, this study establishes a mechanism of action by which PGE counteracts IR-induced colorectal injury as a novel radioprotective agent.
尽管放射治疗(RT)是早期结直肠癌的一种可行治疗方法,但由于活性氧生成增加,RT对正常组织具有相当大的毒性,这会导致组织损伤。人参作为一种天然抗氧化剂,在[具体模型1]和[具体模型2]模型中对电离辐射(IR)诱导的损伤具有保护作用。人参的爆轰膨化已被研究作为一种改善人参功效的方法,因为其功能成分会发生理化变化。在本研究中,我们通过对小鼠模型的研究,提供了膨化人参提取物(PGE)与白参提取物(WGE)相比,在抗IR诱导的结肠损伤方面有益作用增强及其相关作用机制的证据。为了研究PGE在预防IR诱导损伤中的作用,我们检查了暴露于8 Gy Cs的小鼠的结肠损伤和凋亡变化。高效液相色谱分析表明,与WGE中的浓度相比,PGE中总人参皂苷浓度增加,且有新一代的Rg3、Rg5和Rk1。给予PGE而非WGE可通过负调控凋亡信号通路显著改善IR诱导的结肠细胞死亡。PGE的这些抗凋亡作用与抑制p53介导的DNA损伤反应和NF-κB介导的凋亡信号的能力有关。此外,给予PGE可显著降低IR诱导的结肠上皮氧化应激。总体而言,本研究确立了PGE作为一种新型辐射防护剂对抗IR诱导的结肠损伤的作用机制。