Advanced glycation end products induce neural tube defects through elevating oxidative stress in mice
Ru-Lin Li
Wei-Wei Zhao
Bing-Yan Gao
摘要：Our previous study showed an association between advanced glycation end products (AGEs) and neural tube defects (NTDs).To understand the molecular mechanisms underlying the effect of AGEs on neural tube development,C57BL/6 female mice were fed for 4 weeks with commercial food containing 3％ advanced glycation end product bovine serum albumin (AGE-BSA) or 3％ bovine serum albumin (BSA) as a control.After mating mice,oxidative stress markers including malondialdehyde and H2O2 were measured at embryonic day 7.5 (E7.5) of gestation,and the level of intracellular reactive oxygen species (ROS) in embryonic cells was determined at E8.5.In addition to evaluating NTDs,an enzyme-linked immunosorbent assay was used to determine the effect of embryonic protein administration on the N-(carboxymethyl) lysine reactivity of acid and carboxyethyl lysine antibodies at E10.5.The results showed a remarkable increase in the incidence of NTDs at E10.5 in embryos of mice fed with AGE-BSA (no hyperglycemia) compared with control mice.Moreover,embryonic protein administration resulted in a noticeable increase in the reactivity of N-(carboxymethyl) lysine and N(e)-(carboxyethyl) lysine antibodies.Malondialdehyde and H2O2 levels in embryonic cells were increased at E7.5,followed by increased intracellular ROS levels at E8.5.Vitamin E supplementation could partially recover these phenomena.Collectively,these results suggest that AGE-BSA could induce NTDs in the absence of hyperglycemia by an underlying mechanism that is at least partially associated with its capacity to increase embryonic oxidative stress levels.
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资助基金：This study was supported by the grant from Shaanxi Technology Committee of China,(No.2013JM4001)
论文发表日期：2018-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：7( 1368-1374 )
英文信息