Arellano-García Laura, Trepiana Jenifer, Martínez J Alfredo, Portillo María P, Milton-Laskibar Iñaki
Nutrition and Obesity Group, Department of Nutrition and Food Science, Faculty of Pharmacy and Lucio Lascaray Research Centre, University of the Basque Country (UPV/EHU), 01006 Vitoria-Gasteiz, Spain.
CIBERobn Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, 28222 Madrid, Spain.
Antioxidants (Basel). 2023 Mar 14;12(3):717. doi: 10.3390/antiox12030717.
Oxidative stress and inflammation are well-known triggers of NAFLD onset and progression. The aim of this study is to compare the potential benefits of a viable probiotic ( GG) and its parabiotic (heat-inactivated) on oxidative stress, inflammation, DNA damage and cell death pathways in the liver of rats featuring diet-induced NAFLD. The consumption of the steatotic diet led to increased final body and liver weights, higher hepatic triacylglycerol content, altered serum transaminase levels and enhanced oxidative and inflammatory status. Administration of the probiotic and the parabiotic partially prevented the body weight increase induced by the steatotic diet, whereas the probiotic caused more effective decreasing hepatic triglyceride content. Sharp but nonstatistically significant decreases in serum transaminase levels were also observed for both treatments. The reduction in antioxidant enzyme activities found in the nontreated animals fed the steatotic diet was partially prevented by both treatments (GPx activity). Similarly, the reductions in nonenzymatic antioxidant protection (GSH content) and total antioxidant capacity (ORAC) found in the nontreated rats were restored by the administration of both treatments. These results show that both viable and heat-inactivated GG administration partially prevent steatotic diet-induced liver oxidative stress and inflammation induced in rats.
氧化应激和炎症是众所周知的非酒精性脂肪性肝病(NAFLD)发病和进展的触发因素。本研究的目的是比较一种活的益生菌(GG)及其共生菌(热灭活)对饮食诱导的NAFLD大鼠肝脏氧化应激、炎症、DNA损伤和细胞死亡途径的潜在益处。食用脂肪变性饮食导致最终体重和肝脏重量增加、肝脏三酰甘油含量升高、血清转氨酶水平改变以及氧化和炎症状态增强。益生菌和共生菌的给药部分阻止了脂肪变性饮食诱导的体重增加,而益生菌更有效地降低了肝脏甘油三酯含量。两种治疗方法还观察到血清转氨酶水平急剧但无统计学意义的下降。两种治疗方法都部分阻止了喂食脂肪变性饮食的未治疗动物中发现的抗氧化酶活性的降低(谷胱甘肽过氧化物酶活性)。同样,两种治疗方法的给药都恢复了未治疗大鼠中发现的非酶抗氧化保护(谷胱甘肽含量)和总抗氧化能力(氧自由基吸收能力)的降低。这些结果表明,给予活的和热灭活的GG均可部分预防脂肪变性饮食诱导的大鼠肝脏氧化应激和炎症。