Chemico-Biological Interactions, Journal Year: 2023, Volume and Issue: 376, P. 110461 - 110461
Published: March 23, 2023
Language: Английский
Chemico-Biological Interactions, Journal Year: 2023, Volume and Issue: 376, P. 110461 - 110461
Published: March 23, 2023
Language: Английский
Nature reviews. Cancer, Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 1, 2024
Language: Английский
Citations
9Nutrients, Journal Year: 2024, Volume and Issue: 16(17), P. 2838 - 2838
Published: Aug. 24, 2024
The gut microbiota constitutes a complex ecosystem, comprising trillions of microbes that have co-evolved with their host over hundreds millions years. Over the past decade, growing body knowledge has underscored intricate connections among diet, microbiota, and human health. Bioactive polysaccharides (BPs) from natural sources like medicinal plants, seaweeds, fungi diverse biological functions including antioxidant, immunoregulatory, metabolic activities. Their effects are closely tied to which metabolizes BPs into health-influencing compounds. Understanding how interact is critical for harnessing potential health benefits. This review provides an overview focusing on its role in diseases obesity, type II diabetes mellitus, non-alcoholic fatty liver disease, cardiovascular diseases. It explores basic characteristics several impact microbiota. Given significance health, we summarize these BPs, particularly terms immunoregulatory activities, blood sugar, hypolipidemic effect, thus providing valuable reference understanding benefits treating These properties make promising agents preventing comprehensive mechanisms by exert through opens new avenues developing targeted therapies improve
Language: Английский
Citations
8Microorganisms, Journal Year: 2025, Volume and Issue: 13(2), P. 241 - 241
Published: Jan. 23, 2025
The gut microbiota has emerged as a critical player in metabolic and liver health, with its influence extending to the pathogenesis progression of steatotic diseases. This review delves into gut-liver axis, dynamic communication network linking microbiome through metabolic, immunological, inflammatory pathways. Dysbiosis, characterized by altered microbial composition, contributes significantly development hepatic steatosis, inflammation, fibrosis via mechanisms such barrier dysfunction, metabolite production, systemic inflammation. Dietary patterns, including Mediterranean diet, are highlighted for their role modulating microbiota, improving axis integrity, attenuating injury. Additionally, emerging microbiota-based interventions, fecal transplantation bacteriophage therapy, show promise therapeutic strategies disease. However, challenges population heterogeneity, methodological variability, knowledge gaps hinder translational application current findings. Addressing these barriers standardized approaches integrative research will pave way microbiota-targeted therapies mitigate global burden
Language: Английский
Citations
1Biology, Journal Year: 2022, Volume and Issue: 11(11), P. 1622 - 1622
Published: Nov. 6, 2022
Non-alcoholic fatty liver disease (NAFLD) is a prevalent, multifactorial, and poorly understood with an increasing incidence worldwide. NAFLD typically asymptomatic coupled other symptoms of metabolic syndrome. The prevalence rising in tandem the obesity. In Western hemisphere, one most prevalent causes transplantation. Recent research suggests that gut microbiome dysbiosis may play significant role pathogenesis by dysregulating gut–liver axis. so-called “gut–liver axis” refers to communication feedback loop between digestive system liver. Several pathological mechanisms characterized alteration axis, such as impairment barrier increase intestinal permeability which result endotoxemia inflammation, changes bile acid profiles metabolite levels produced microbiome. This review will explore axis disruption, mediated dysbiosis, on development.
Language: Английский
Citations
31Frontiers in Medicine, Journal Year: 2022, Volume and Issue: 9
Published: March 3, 2022
Cirrhosis and liver cancer caused by alcohol-associated disease (ALD) are serious threats to people's health. In addition hepatic cell apoptosis inflammation oxidative stress during alcohol metabolism, intestinal microbiota disorders also involved in the onset development of ALD. Ethanol its' non-oxidative metabolites, together with dysbiosis-caused-inflammation, destroys barrier. Changes several microbial such as bile acids, short-chain fatty amino acid, closely associated gut dysbiosis The alcohol-caused can further influence barrier-related proteins, mucin2, acid-related receptors, aryl hydrocarbon receptor (AhR), these abnormal changes participate injury barrier steatosis. Gut-derived bacteria, fungi, their toxins, lipopolysaccharide (LPS) β-glucan translocate into through damaged promote progression fibrosis Thus, prevention alcohol-induced disruption permeability has a beneficial effect on Currently, multiple therapeutic treatments have been applied restore patients Fecal transplantation, probiotics, antibiotics, many other elements already shown ability restoring microbiota. Targeted approaches, using bacteriophages remove cytolytic Enterococcus faecalis , supplement Lactobacillus, Bifidobacterium or boulardii powerful options for
Language: Английский
Citations
30Frontiers in Microbiology, Journal Year: 2022, Volume and Issue: 13
Published: June 13, 2022
Lipopolysaccharide (LPS), a gut-transmitted endotoxin from Gram-negative bacteria, causes inflammatory diseases leading to the loss of gut barrier integrity and has been identified as major pathogenic stimulator in many dysfunctions. Hence, supplementation with probiotics is believed be one most effective strategies for treating disorders. Although are known have variety therapeutic characteristics play beneficial role host defense responses, molecular mechanisms by which they achieve these effects unknown due species- strain-specific behaviors. Therefore, this study, protective five indigenous lactic acid bacterial strains ameliorating LPS-induced impairment C57BL/6 mice model was elucidated. Lacticaseibacillus rhamnosus LAB3, Levilactobacillus brevis LAB20, Lactiplantibacillus plantarum LAB31 were isolated infant feces; Pediococcus acidilactici LAB8 fermented food (Bekang); LAB39 beetroot. Intraperitoneal injection LPS (10 mg/kg body weight) increased levels lipocalin serum markers TNF-α, IL-6, IL-1β, overall disease activity index treated group. Furthermore, gene expression NF-kB, IL-12, Cox-2; mucin-producing genes Muc-2 Muc-4; intestinal alkaline phosphatase (IAP) deleteriously altered ileum LPS-treated mice. also induced dysbiosis microbiota where higher abundances Klebsiella, Enterobacter, Salmonella decreased Lactobacillus, Bifidobacteria, Roseburia, Akkermansia observed. Western blotting results suggested that treatment relative pre-supplementation LAB strains, enhanced tight junction proteins ameliorated changes inflammation. Taken together, study LAB3 more potent inflammation dysbiosis.
Language: Английский
Citations
29Nutrients, Journal Year: 2023, Volume and Issue: 15(3), P. 687 - 687
Published: Jan. 29, 2023
While non-alcoholic fatty liver disease (NAFLD) is a prevalent and frequent cause of liver-related morbidity mortality, it also strongly associated with cardiovascular disease-related likely driven by its associations insulin resistance other manifestations metabolic dysregulation. However, few satisfactory pharmacological treatments are available for NAFLD due in part to complex pathophysiology, challenges remain stratifying individual patient’s risk related outcomes. In this review, we describe the development progression NAFLD, including pathophysiology We different tools identifying patients who most at cardiovascular-related complications, as well current emerging treatment options, future directions research.
Language: Английский
Citations
22Nutrients, Journal Year: 2023, Volume and Issue: 15(3), P. 743 - 743
Published: Feb. 1, 2023
The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is bioactive compound found cruciferous vegetables; however, it not been reported whether SFN improves NAFLD via axis. C57BL/6 mice were fed high-fat and high-fructose (HFHFr) diet, with or without gavage at doses 15 30 mg·kg−1 body weight for 12 weeks. results showed that reduced gain, hepatic inflammation, steatosis HFHFr mice. altered composition gut microbes. Moreover, enhanced intestinal tight junction protein ZO-1, serum LPS, inhibited LPS/TLR4 ERS pathways to reduce inflammation. As result, protected integrity declined gut-derived LPS translocations diet-induced decreased levels pathway activations, thus inhibiting pro-inflammatory cytokines. Notably, Spearman correlation analysis protective effect on barrier its anti-inflammatory was associated improved dysbiosis. Above all, dietary intervention attenuates through
Language: Английский
Citations
20Metabolites, Journal Year: 2023, Volume and Issue: 13(1), P. 101 - 101
Published: Jan. 7, 2023
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disease, ranging from simple steatosis to hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Liver which portends poor prognosis in NAFLD, characterized by the excessive accumulation extracellular matrix (ECM) proteins resulting abnormal wound repair response metabolic disorders. Various factors play crucial roles progression including lipid, bile acid, endotoxin metabolism, leading chronic inflammation hepatic stellate cell (HSC) activation. Autophagy conserved process within cells that removes unnecessary or dysfunctional components through lysosome-dependent regulated mechanism. Accumulating evidence has shown importance autophagy NAFLD its close relation progression. Thus, regulation appears be beneficial treating could become an important therapeutic target.
Language: Английский
Citations
19International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(6), P. 5465 - 5465
Published: March 13, 2023
Mitophagy/autophagy plays a protective role in various forms of liver damage, by renovating cellular metabolism linking to sustain homeostasis. A characterized pathway for mitophagy is the phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkin-dependent signaling pathway. In particular, PINK1-mediated could play an indispensable improving metabolic dysfunction-associated fatty disease (MAFLD) which precede steatohepatitis (NASH), fibrosis, hepatocellular carcinoma. addition, PI3K/AKT/mTOR might regulate characteristics homeostasis including energy metabolism, cell proliferation, and/or protection. Therefore, targeting with alteration or PINK1/Parkin-dependent eliminate impaired mitochondria be attractive strategy treatment MAFLD. efficacy prebiotics MAFLD has been suggested useful via modulation PI3K/AKT/mTOR/AMPK Additionally, several edible phytochemicals activate improvement mitochondrial damages, also promising option treat providing Here, potential therapeutics discussed Tactics viewpoint prospective probiotics contribute development therapeutic interventions.
Language: Английский
Citations
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