Hydrogen inhalation ameliorates hepatic inflammation and modulates gut microbiota in rats with high-fat diet-induced non-alcoholic fatty liver disease

Xue, Junli; Zhao, Min; Liu, Yunchao; Jia, Xiubin; Zhang, Xiaoyi; Gu, Qianqian; Xie, Yunbo; Qin, Shucun; Liu, Boyan

doi:10.1016/j.ejphar.2023.175698

Cited by 6 publications

(5 citation statements)

References 44 publications

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“…Activation of the NF-κB pathway is crucial to the inflammatory response in the NAFLD liver and can regulate the expression of various inflammation-related factors [35,36]. NF-κB can be regulated by various inflammatory factors, such as TNF-α and IL-1β.…”

Section: Discussionmentioning

confidence: 99%

Glucosamine Improves Non-Alcoholic Fatty Liver Disease Induced by High-Fat and High-Sugar Diet through Regulating Intestinal Barrier Function, Liver Inflammation, and Lipid Metabolism

Li,

Zhang,

Bai

et al. 2023

Molecules

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Non-alcoholic fatty liver disease (NAFLD) is a liver disease syndrome. The prevalence of NAFLD has continued to increase globally, and NAFLD has become a worldwide public health problem. Glucosamine (GLC) is an amino monosaccharide derivative of glucose. GLC has been proven to not only be effective in anti-inflammation applications, but also to modulate the gut microbiota effectively. Therefore, in this study, the therapeutic effect of GLC in the NAFLD context and the mechanisms underlying these effects were explored. Specifically, an NAFLD model was established by feeding mice a high-fat and high-sugar diet (HFHSD), and the HFHSD-fed NAFLD mice were treated with GLC. First, we investigated the effect of treating NAFLD mice with GLC by analyzing serum- and liver-related indicator levels. We found that GLC attenuated insulin resistance and inflammation, increased antioxidant function, and attenuated serum and liver lipid metabolism in the mice. Then, we investigated the mechanism underlying liver lipid metabolism, inflammation, and intestinal barrier function in these mice. We found that GLC can improve liver lipid metabolism and relieve insulin resistance and oxidative stress levels. In addition, GLC treatment increased intestinal barrier function, reduced LPS translocation, and reduced liver inflammation by inhibiting the activation of the LPS/TLR4/NF-κB pathway, thereby effectively ameliorating liver lesions in NAFLD mice.

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Section: Discussionmentioning

confidence: 99%

Glucosamine Improves Non-Alcoholic Fatty Liver Disease Induced by High-Fat and High-Sugar Diet through Regulating Intestinal Barrier Function, Liver Inflammation, and Lipid Metabolism

Li,

Zhang,

Bai

et al. 2023

Molecules

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“…Necrotizing Enterocolitis [63] Alloprevotella，bacterium_f_Muribaculaceae LPS/TLR4/NF-κB signaling pathway Nonalcoholic fatty liver disease [64] Akkermansia, Lactobacillus, and A2. TLR2/NLRP3 signaling pathway…”

Section: Gut Microbiota-tlrs Interaction In Crcmentioning

confidence: 99%

Interactions between toll‐like receptors signaling pathway and gut microbiota in host homeostasis

Chen,

Zhang,

Hua

et al. 2024

Immunity Inflam & Disease

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BackgroundToll‐like receptors (TLRs) are a family of fundamental pattern recognition receptors in the innate immune system, constituting the first line of defense against endogenous and exogenous antigens. The gut microbiota, a collection of commensal microorganisms in the intestine, is a major source of exogenous antigens. The components and metabolites of the gut microbiota interact with specific TLRs to contribute to whole‐body immune and metabolic homeostasis.ObjectiveThis review aims to summarize the interaction between the gut microbiota and TLR signaling pathways and to enumerate the role of microbiota dysbiosis‐induced TLR signaling pathways in obesity, inflammatory bowel disease (IBD), and colorectal cancer (CRC).ResultsThrough the recognition of TLRs, the microbiota facilitates the development of both the innate and adaptive immune systems, while the immune system monitors dynamic changes in the commensal bacteria to maintain the balance of the host‐microorganism symbiosis. Dysbiosis of the gut microbiota can induce a cascade of inflammatory and metabolic responses mediated by TLR signaling pathways, potentially resulting in various metabolic and inflammatory diseases.ConclusionUnderstanding the crosstalk between TLRs and the gut microbiota contributes to potential therapeutic applications in related diseases, offering new avenues for treatment strategies in conditions like obesity, IBD, and CRC.

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“…As indicated by various preclinical studies, extrinsic hydrogen supplementation leads to increase in the abundance of Lachnospiraceae, 102,103 Lactobacillus, 101,104 Ruminococcus, 101 Clostridia, 101,102 Akkermansia, 16 Firmicutes, 105 Actinobacteria, 106 and Bifidobacteria, 104 and decrease in the abundance of Bacteroides, 101,105,107 Blautia, 101 Paraprevotella, 101 Prevotellaceae, 102 Muribaculaceae, 102 Enterococcus, 107 Escherichia 108 and Enterobacteriaceae. 103 Through increasing beneficial bacteria while suppressing pernicious bacteria, the modulated microbiota can promote immune and metabolism homeostasis through modulating metabolism processes.…”

Section: Hydrogen Therapy In Modulating Gut Microbiotamentioning

confidence: 99%

“…[109][110][111] Moreover, microbiota alteration can also affect brain function through the gut-brain axis through a complex mechanism. 112 So far, the modulation of microbiota was indicated as a part of the mechanism of hydrogen treatment, and has shown potential for treating alcoholic hepatitis, 102 NAFLD, 16,105 IBD, 107 colitis, 108 muscle fatigue, 113 cholangiofibrosis, 114 metabolic syndrome, 104 diabetes mellitus, 115 and sepsis. 103,116…”

Section: Hydrogen Therapy In Modulating Gut Microbiotamentioning

confidence: 99%

Hydrogen therapy: recent advances and emerging materials

Jiang,

Ainiwaer,

Liu

et al. 2024

Biomater. Sci.

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Hydrogen inhalation ameliorates hepatic inflammation and modulates gut microbiota in rats with high-fat diet-induced non-alcoholic fatty liver disease

Cited by 6 publications

References 44 publications

Glucosamine Improves Non-Alcoholic Fatty Liver Disease Induced by High-Fat and High-Sugar Diet through Regulating Intestinal Barrier Function, Liver Inflammation, and Lipid Metabolism

Glucosamine Improves Non-Alcoholic Fatty Liver Disease Induced by High-Fat and High-Sugar Diet through Regulating Intestinal Barrier Function, Liver Inflammation, and Lipid Metabolism

Interactions between toll‐like receptors signaling pathway and gut microbiota in host homeostasis

Hydrogen therapy: recent advances and emerging materials

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