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Accumulation and effects of dietary advanced glycation end products on the gastrointestinal tract in rats

机译:膳食高级糖基化终产物在大鼠胃肠道的积累及其作用

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摘要

The gastrointestinal (GI) tract represents the first barrier against the penetration of organisms by dietary advanced glycation end products (AGEs), but the tissue accumulation of AGEs and AGE-induced effects on the GI tract have yet to be completely elucidated. This study aimed to investigate the tissue accumulation of AGEs and AGE-induced oxidative stress and inflammation in the GI tract of rats after long-term consumption of AGEs from bread crust (BC). The GI tract was then removed to analyse car-boxymethyllysine (CML) and malondialdehyde (MDA) contents, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). This study demonstrates that the oral intake of AGEs promotes their accumulation in the GI tract, and AGEs attenuate the first-line antioxidant defence and stimulate the inflammatory response of the GI tract by downregulating enzymatic antioxidative pathways and increasing inflammatory cytokine levels.
机译:胃肠道(GI)代表饮食高级糖基化终末产物(AGEs)阻止生物渗透的第一个障碍,但是尚未完全阐明AGEs的组织蓄积和AGE对GI道的影响。这项研究的目的是调查从面包壳(BC)长期摄入AGEs后,大鼠胃肠道中AGEs的组织积累以及AGE诱导的氧化应激和炎症。然后取出胃肠道以分析羧甲基赖氨酸(CML)和丙二醛(MDA)含量,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性以及肿瘤坏死因子-α(TNF-α)的水平)和白介素6(IL-6)。这项研究表明,口服AGEs可以促进其在GI道中的积累,而AGEs通过下调酶促抗氧化途径和增加炎症细胞因子水平来减弱一线抗氧化防御并刺激GI道的炎症反应。

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