El-Masry Thanaa A, Al-Shaalan Nora H, Tousson Ehab, Buabeid Manal, Alyousef Anhar M
Pharmaceutical Science Department, College of Pharmacy, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia/Departement of Pharmacology and Toxicology, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
Chemistry Department, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Pak J Pharm Sci. 2019 Nov;32(6(Supplementary)):2801-2810.
Many cancer therapies indirectly activate apoptosis by chemical or physical damage of DNA. This study was performed to evaluate protective potential of vitamin B17 (VitB17) against Ehrlich solid tumor (EST) induced changes in the oxidative stress, DNA damage, apoptosis and proliferation in mice. In the experiment, 60 female CD1 mice were randomly and allocated to the following four equal-sized groups [G1, negative control; G2, positive control (VitB17); G3, untreated EST; G4, EST treated with VitB17 (EST+VitB17)]. The untreated EST group displayed major increases in tumor volume, significant increase in the levels of MDA, HO, NO, PCNA, TNF-α, AFP and dsDNA and notable reductions in the catalase, GSH, P53 and SOD activities. By contrast, reduced levels of TNF-α, AFP, MDA, HO, NO, PCNA and dsDNA, along with enhanced levels of P53 and the antioxidant indicators catalase, GSH and SOD were observed in the EST+VitB17 group. These results indicate the antineoplastic and antioxidant properties of vitamin B17 with the potential to decrease the oxidative stress associated with ESTs by augmenting the antioxidant defence system.
许多癌症疗法通过对DNA的化学或物理损伤间接激活细胞凋亡。本研究旨在评估维生素B17(VitB17)对艾氏实体瘤(EST)诱导的小鼠氧化应激、DNA损伤、细胞凋亡和增殖变化的保护潜力。实验中,60只雌性CD1小鼠被随机分为以下四个等大小的组[G1,阴性对照组;G2,阳性对照组(VitB17);G3,未治疗的EST组;G4,用VitB17治疗的EST组(EST+VitB17)]。未治疗的EST组肿瘤体积大幅增加,丙二醛(MDA)、羟基自由基(HO)、一氧化氮(NO)、增殖细胞核抗原(PCNA)、肿瘤坏死因子-α(TNF-α)、甲胎蛋白(AFP)和双链DNA(dsDNA)水平显著升高,而过氧化氢酶、谷胱甘肽(GSH)、P53和超氧化物歧化酶(SOD)活性显著降低。相比之下,EST+VitB17组中TNF-α、AFP、MDA、HO、NO、PCNA和dsDNA水平降低,同时P53以及抗氧化指标过氧化氢酶、GSH和SOD水平升高。这些结果表明维生素B17具有抗肿瘤和抗氧化特性,有可能通过增强抗氧化防御系统来降低与EST相关的氧化应激。