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Inhibiting nuclear factor erythroid 2 related factor 2-mediated autophagy in bovine mammary epithelial cells induces oxidative stress in response to exogenous fatty acids

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Journal of Animal Science and Biotechnology 2022年第5期13卷 1458-1468页

作者： Renxu Chang Xudong Sun hongdou jia Qiushi Xu Zhihao Dong Yan Tang Shengbin Luo Qianming jiang Juan J.Loor Chuang Xu College of Veterinary Medicine China Agricultural UniversityYuan Ming Yuan West Road No.2Haidian DistrictBeijing 100193China College of Veterinary Medicine Hunan Agricultural UniversityChangsha 410128China Heilongjiang Provincial Key Laboratory of Prevention and Control of Bovine Diseases College of Animal Science and Veterinary MedicineHeilongjiang Bayi Agricultural UniversityNo.5 Xinyang RoadDaqing 163319Heilongjiang ProvinceChina Mammalian NutriPhysioGenomics Department of Animal Sciences and Division of Nutritional SciencesUniversity of IllinoisUrbana 61801USA

Background:In early lactation,bovine mammary epithelial cells undergo serious metabolic challenges and oxidative stress both of which could be alleviated by activation of autophagy.Nuclear factor erythroid 2 related factor 2(NFE2L2),a master regulator of cellular redox homeostasis,plays an important role in the regulation of autophagy and oxidative stress.Thus,the objective of this study was to investigate the role of NFE2L2-mediated autophagy on oxidative stress of bovine mammary epithelial cells in response to exogenous free fatty acids(FFA).Results:Exogenous FFA induced linear and quadratic decreases in activities of glutathione peroxidase(GSH-Px),catalase(CAT),and superoxide dismutase(SOD),and increases in the contents of reactive oxygen species(ROS)and malondialdehyde(MDA).Protein abundance of LC3-phosphatidylethanolamine conjugate(LC3-Ⅱ)and the number of autophagosomes and autolysosomes decreased in a dose-dependent manner,while protein abundance of p62 increased in cells challenged with FFA.Activation of autophagy via pre-treatment with Rap attenuated the FFAinduced ROS accumulation.Importantly,FFA inhibited protein abundance of NFE2L2 and the translocation of NFE2L2 into the nucleus.Knockdown of NFE2L2 by siRNA decreased protein abundance of LC3-Ⅱ,while it increased protein abundance of p62.Furthermore,sulforaphane(SFN)pre-treatment attenuated the FFA-induced oxidative stress by activating NFE2L2-mediated autophagy.Conclusions:The data suggested that NFE2L2-mediated autophagy is an important antioxidant mechanism in bovine mammary epithelial cells experiencing increased FFA loads.

关键词： Autophagy Bovine mammary epithelial cells NFE2L2 Oxidative stress

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维普期刊数据库

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Transcription factor EB(TFEB)-mediated autophagy protects bovine mammary epithelial cells against H_(2)O_(2)-induced oxidative damage in vitro

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Journal of Animal Science and Biotechnology 2021年第3期12卷 1008-1018页

作者： Xudong Sun Renxu Chang Yan Tang Shengbin Luo Chunhui jiang hongdou jia Qiushi Xu Zhihao Dong Yusheng Liang Juan J.Loor Chuang Xu Heilongjiang Provincial Key Laboratory of Prevention and Control of Bovine Diseases College of Animal Science and Veterinary MedicineHeilongjiang Bayi Agricultural UniversityNo.5 Xinyang RoadDaqing 163319Heilongjiang ProvinceChina College of Veterinary Medicine Hunan Agricultural UniversityChangsha 410128China Mammalian NutriPhysioGenomics Department of Animal Sciences and Division of Nutritional SciencesUniversity of IllinoisUrbana 61801USA

Background:Bovine mammary epithelial cells after calving undergo serious metabolic challenges and oxidative stress both of which could compromise autophagy.Transcription factor EB(TFEB)-mediated autophagy is an important cytoprotective mechanism against oxidative stress.However,effects of TFEB-mediated autophagy on the oxidative stress of bovine mammary epithelial cells remain unknown.Therefore,the main aim of the study was to investigate the role of TFEB-mediated autophagy in bovine mammary epithelial cells experiencing oxidative stress.Results:H_(2)O_(2) challenge of the bovine mammary epithelial cell MAC-T increased protein abundance of LC3-II,increased number of autophagosomes and autolysosomes while decreased protein abundance of p62.Inhibition of autophagy via bafilomycin A1 aggravated H_(2)O_(2)-induced reactive oxygen species(ROS)accumulation and apoptosis in MAC-T cells.Furthermore,H_(2)O_(2) treatment triggered the translocation of TFEB into the nucleus.Knockdown of TFEB by siRNA reversed the effect of H_(2)O_(2) on protein abundance of LC3-II and p62 as well as the number of autophagosomes and autolysosomes.Overexpression of TFEB activated autophagy and attenuated H_(2)O_(2)-induced ROS accumulation.Furthermore,TFEB overexpression attenuated H_(2)O_(2)-induced apoptosis by downregulating the caspase apoptotic pathway.Conclusions:Our results indicate that activation of TFEB mediated autophagy alleviates H_(2)O_(2)-induced oxidative damage by reducing ROS accumulation and inhibiting caspase-dependent apoptosis.

关键词： Apoptosis Autophagy Bovine mammary epithelial cells Oxidative stress TFEB

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茶多酚通过NF-κB通路缓解LPS诱导的奶牛乳腺上皮细胞炎性反应

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中国兽医学报 2021年第7期41卷 1372-1375页

作者：贾红豆黑龙江八一农垦大学生物技术中心黑龙江大庆163319

为了探讨茶多酚对脂多糖(lipopolysaccharide, LPS)诱导的奶牛乳腺上皮细胞炎性反应的影响,本试验使用LPS(1 mg/L)和或茶多酚(50,100,200 mg/L)处理奶牛乳腺上皮细胞(MAC-T),随后采用ELISA试剂盒、Western blot方法和实时荧光定量PCR方... 详细信息

为了探讨茶多酚对脂多糖(lipopolysaccharide, LPS)诱导的奶牛乳腺上皮细胞炎性反应的影响,本试验使用LPS(1 mg/L)和或茶多酚(50,100,200 mg/L)处理奶牛乳腺上皮细胞(MAC-T),随后采用ELISA试剂盒、Western blot方法和实时荧光定量PCR方法检测NF-κB信号通路关键分子及下游靶基因的表达变化。结果显示,与LPS组相比,茶多酚+LPS组中IKK-β活性显著降低,IκB-α和NF-κB的磷酸化水平也显著降低。此外,茶多酚+LPS组中TNF-α、IL-6和IL-1βmRNA表达量也显著低于LPS组。结果表明,茶多酚可以通过抑制NF-κB炎性信号通路缓解LPS诱导的奶牛乳腺上皮细胞炎性反应。

关键词：奶牛脂多糖茶多酚乳腺上皮细胞

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