食品科学与人类健康(英文)2024,Vol.13Issue(3) :1475-1484.DOI:10.26599/FSHW.2022.9250124

Procyanidin A1 and its digestive products alleviate acrylamide-induced IPEC-J2 cell damage through regulating Keap1/Nrf2 pathway

Fangfang Yan Qun Lu Chengming Wang Rui Liu
食品科学与人类健康(英文)2024,Vol.13Issue(3) :1475-1484.DOI:10.26599/FSHW.2022.9250124

Procyanidin A1 and its digestive products alleviate acrylamide-induced IPEC-J2 cell damage through regulating Keap1/Nrf2 pathway

Fangfang Yan 1Qun Lu 2Chengming Wang 2Rui Liu3
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作者信息

  • 1. College of Food Science and Technology,Huazhong Agricultural University,Wuhan 430070,China
  • 2. College of Food Science and Technology,Huazhong Agricultural University,Wuhan 430070,China;Key Laboratory of Environment Correlative Dietology(Huazhong Agricultural University),Ministry of Education,Wuhan 430070,China
  • 3. College of Food Science and Technology,Huazhong Agricultural University,Wuhan 430070,China;Key Laboratory of Environment Correlative Dietology(Huazhong Agricultural University),Ministry of Education,Wuhan 430070,China;Key Laboratory of Urban Agriculture in Central China,Ministry of Agriculture and Rural Affairs,Wuhan 430070,China
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Abstract

Our previous study has revealed that procyanidin A1(A1)and its simulated digestive product(D-A1)can alleviate acrylamide(ACR)-induced intestine cell damage.However,the underlying mechanism remains unknown.In this study,we elucidated the molecular mechanism for A1 and D-A1 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.A1 and D-A1 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 A1 and D-A1 interacted with Kelch-like ECH-associated protein 1(Keap1),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 A1 and D-A1 treated groups,indicating that A1 can tolerate gastrointestinal digestion and may be a potential compound to limit the toxicity of ACR.

Key words

Procyanidin A1/Digestive products/Acrylamide/Nuclear factor erythroid 2-related factor 2(Nrf2)/Intestinal cell damage

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基金项目

国家自然科学基金(31671962)

中央高校基本科研业务费专项(2662019PY034)

出版年

2024
食品科学与人类健康(英文)

食品科学与人类健康(英文)

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