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      Lactobacillus plantarum KSFY06 Prevents Inflammatory Response and Oxidative Stress in Acute Liver Injury Induced by D-Gal/LPS in Mice

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          The purpose of this study is to investigate the preventive effect of Lactobacillus plantarum KSFY06 (LP-KSFY06) on D-galactose/lipopolysaccharide (D-Gal/LPS)-induced acute liver injury (ALI) in mice.


          We evaluated the antioxidant capacity of LP-KSFY06 in vitro, detailed the effects of LP-KSFY06 on the organ index, liver function index, biochemical index, cytokines, and related genes, and noted the accompanying pathological changes.


          The results clearly showed that LP-KSFY06 can remove 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzthiazoline −6-sulphonic acid) diammonium salt (ABTS) free radicals in vitro. The analysis of the organ index and pathology demonstrated that LP-KSFY06 significantly prevented ALI. Biochemical and molecular biological analysis showed that LP-KSFY06 prevented a decrease in the antioxidant-related levels of superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px), catalase (CAT), and total antioxidant capacity (T-AOC), and also prevented an increase in aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), malondialdehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) levels. LP-KSFY06 upregulated the anti-inflammatory factor interleukin (IL)-10 and downregulated the pro-inflammatory factors IL-6, IL-1β, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). These oxidative and inflammatory indicators were consistent with the results of gene detections. Furthermore, we determined that LP-KSFY06 downregulated Keap1, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), IL-18, and mitogen-activated protein kinase 14 (MAPK14 or p38), upregulated Nrf2, heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase [quinone] 1 (NQO1), B-cell inhibitor-α (IκB-α), and thioredoxin (Trx) mRNA expression. These may be related to the regulation of the Kelch-like ECH-associated protein-1 (Keap1)-nuclear factor-erythroid-2-related factor (Nrf2)/antioxidant response element (ARE) and NLRP3/NF-κB pathways.


          LP-KSFY06 is an effective multifunctional Lactobacillus with strong anti-oxidant and anti-inflammatory ability that can prevent D-gal/LPS-induced ALI in mice and assist in maintaining health.

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              Oxidative stress, aging, and diseases

              Reactive oxygen and nitrogen species (RONS) are produced by several endogenous and exogenous processes, and their negative effects are neutralized by antioxidant defenses. Oxidative stress occurs from the imbalance between RONS production and these antioxidant defenses. Aging is a process characterized by the progressive loss of tissue and organ function. The oxidative stress theory of aging is based on the hypothesis that age-associated functional losses are due to the accumulation of RONS-induced damages. At the same time, oxidative stress is involved in several age-related conditions (ie, cardiovascular diseases [CVDs], chronic obstructive pulmonary disease, chronic kidney disease, neurodegenerative diseases, and cancer), including sarcopenia and frailty. Different types of oxidative stress biomarkers have been identified and may provide important information about the efficacy of the treatment, guiding the selection of the most effective drugs/dose regimens for patients and, if particularly relevant from a pathophysiological point of view, acting on a specific therapeutic target. Given the important role of oxidative stress in the pathogenesis of many clinical conditions and aging, antioxidant therapy could positively affect the natural history of several diseases, but further investigation is needed to evaluate the real efficacy of these therapeutic interventions. The purpose of this paper is to provide a review of literature on this complex topic of ever increasing interest.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                06 January 2021
                : 15
                : 37-50
                [1 ]Chongqing Collaborative Innovation Center for Functional Food, Chongqing University of Education , Chongqing 400067, People’s Republic of China
                [2 ]Chongqing Engineering Research Center of Functional Food, Chongqing University of Education , Chongqing 400067, People’s Republic of China
                [3 ]Chongqing Engineering Laboratory for Research and Development of Functional Food, Chongqing University of Education , Chongqing 400067, People’s Republic of China
                [4 ]Pre-Hospital Emergency Department, Chongqing University Central Hospital, Chongqing Emergency Medical Center , Chongqing 400014, People’s Republic of China
                [5 ]Department of Public Health, Our Lady of Fatima University , Valenzuela 838, Philippines
                Author notes
                Correspondence: Xin Zhao; Kun-Young Park Tel +86-23-6265-3650 Email zhaoxin@cque.edu; kunypark@foods.ac.cn

                These authors contributed equally to this work

                © 2021 Li et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 8, Tables: 7, References: 62, Pages: 14
                Original Research


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