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作 者:Fangfang Yan Qun Lu Chengming Wang Rui Liu
机构地区:[1]College of Food Science and Technology,Huazhong Agricultural University,Wuhan 430070,China [2]Key Laboratory of Environment Correlative Dietology(Huazhong Agricultural University),Ministry of Education,Wuhan 430070,China [3]Key Laboratory of Urban Agriculture in Central China,Ministry of Agriculture and Rural Affairs,Wuhan 430070,China
出 处:《Food Science and Human Wellness》2024年第3期1475-1484,共10页食品科学与人类健康(英文)
基 金:supported by the project from National Natural Science Foundation of China (31671962);Fundamental Research Funds for the Central Universities (2662019PY034)。
摘 要:Our previous study has revealed that procyanidin A_(1)(A_(1))and its simulated digestive product(D-A,)can alleviate acrylamide(ACR)-induced intestine cell damage.However,the underlying mechanism remains unknown.In this study,we elucidated the molecular mechanism for and D-A_(1) to alleviate ACR-stimulated IPEC-J2 cell damage.ACR slightly activated nuclear factor erythroid 2-related factor 2(Nrf2)signaling and its target genes,but this activation could not reduce intestine cell damage.A_(1) and D-A_(1) could alleviate ACR-induced cell damage,but the effect was abrogated in cells transiently transfected with Nrf2 small interfering RNA(siRNA).Further investigation confirmed that A_(1) and D-A_(1) interacted with Ketch-like ECH-associated protein 1(Keapl),which boosted the stabilization of Nrf2,subsequently promoted the translocation of Nrf2 into the nucleus,and further increased the expression of antioxidant proteins,thereby inhibiting glutathione(GSH)consumption,maintaining redox balance and eventually alleviating ACR-induced cell damage.Importantly,there was no difference between A_(1) and D-A_(1) treated groups,indicating that A_(1) can tolerate gastrointestinal digestion and may be a potential compound to limit the toxicity of ACR.
关 键 词:Procyanidin A_1 Digestive products Acrylamide Nuclear factor erythroid 2-related factor 2(Nrf2) Intestinal cell damage
分 类 号:TS201.6[轻工技术与工程—食品科学]
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