scholarly journals 2′-Fucosyllactose Ameliorates Oxidative Stress Damage in d-Galactose-Induced Aging Mice by Regulating Gut Microbiota and AMPK/SIRT1/FOXO1 Pathway

Foods ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 151
Author(s):  
Jin Wang ◽  
Jia-Qiang Hu ◽  
Yu-Jie Song ◽  
Jia Yin ◽  
Yuan-Yi-Fei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gut Microbiota ◽  
Accelerated Aging ◽  
The Elderly ◽  
Short Chain Fatty Acids ◽  
Mucosal Barrier ◽  
Related Factor ◽  
Mucosal Barrier Function ◽  
Gut Mucosal Barrier ◽  
Stress Damage

The imbalance of reactive oxygen species is the main cause in aging, accompanied by oxidative stress. As the most abundant in human milk oligosaccharides (HMOs), 2′-Fucosyllactose (2′-FL) has been confirmed to have great properties in immunity regulation and anti-inflammatory. The research on 2′-FL is focused on infants currently, while there is no related report of 2′-FL for the elderly. A d-galactose-induced accelerated aging model was established to explore the protective effect of 2′-FL on the intestines and brain in mice. In this study, 2′-FL significantly reduced oxidative stress damage and inflammation in the intestines of aging mice, potentially by regulating the sirtuin1 (SIRT1)-related and nuclear factor E2-related factor 2 (Nrf2) pathways. In addition, 2′-FL significantly improved the gut mucosal barrier function and increased the content of short-chain fatty acids (SCFAs) in the intestine. The gut microbiota analysis indicated that 2′-FL mainly increased the abundance of probiotics like Akkermansia in aging mice. Moreover, 2′-FL significantly inhibited apoptosis in the brains of aging mice, also increasing the expression of SIRT1. These findings provided a basis for learning the benefits of 2′-FL in the aging process.

scholarly journals Central Role of Oxidative Stress in Age-Related Macular Degeneration: Evidence from a Review of the Molecular Mechanisms and Animal Models

2020 ◽  
Vol 2020 ◽  
pp. 1-19 ◽  
Author(s):  
Samuel Abokyi ◽  
Chi-Ho To ◽  
Tim T. Lam ◽  
Dennis Y. Tse
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Macular Degeneration ◽  
Molecular Mechanisms ◽  
The Elderly ◽  
Age Related Macular Degeneration ◽  
Related Factor ◽  
Vascular Endothelial ◽  
Age Related ◽  
Endothelial Growth Factor

Age-related macular degeneration (AMD) is a common cause of visual impairment in the elderly. There are very limited therapeutic options for AMD with the predominant therapies targeting vascular endothelial growth factor (VEGF) in the retina of patients afflicted with wet AMD. Hence, it is important to remind readers, especially those interested in AMD, about current studies that may help to develop novel therapies for other stages of AMD. This study, therefore, provides a comprehensive review of studies on human specimens as well as rodent models of the disease, to identify and analyze the molecular mechanisms behind AMD development and progression. The evaluation of this information highlights the central role that oxidative damage in the retina plays in contributing to major pathways, including inflammation and angiogenesis, found in the AMD phenotype. Following on the debate of oxidative stress as the earliest injury in the AMD pathogenesis, we demonstrated how the targeting of oxidative stress-associated pathways, such as autophagy and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling, might be the futuristic direction to explore in the search of an effective treatment for AMD, as the dysregulation of these mechanisms is crucial to oxidative injury in the retina. In addition, animal models of AMD have been discussed in great detail, with their strengths and pitfalls included, to assist inform in the selection of suitable models for investigating any of the molecular mechanisms.

Effects of Nucleosides and a Nucleotide Mixture on Gut Mucosal Barrier Function on Parenteral Nutrition in Rats

1997 ◽  
Vol 21 (2) ◽  
pp. 104-111 ◽  
Author(s):  
Masanori Kishibuchi ◽  
Toshimasa Tsujinaka ◽  
Masahiko Yano ◽  
Takashi Morimoto ◽  
Shohei Jima ◽  
...  
Keyword(s):  
Parenteral Nutrition ◽  
Barrier Function ◽  
Mucosal Barrier ◽  
Mucosal Barrier Function ◽  
Gut Mucosal Barrier

scholarly journals Ramulus Mori (Sangzhi) Alkaloids (SZ-A) Ameliorate Glucose Metabolism Accompanied by the Modulation of Gut Microbiota and Ileal Inflammatory Damage in Type 2 Diabetic KKAy Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Quan Liu ◽  
Shuainan Liu ◽  
Hui Cao ◽  
Wenming Ji ◽  
Caina Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Insulin Response ◽  
Mucosal Barrier ◽  
Inflammatory Damage ◽  
Kkay Mice ◽  
Mucosal Barrier Function

The novel Traditional Chinese Medicine Ramulus Mori (Sangzhi) alkaloid tablets (SZ-A) are approved by The China National Medical Products Administration for the treatment of type 2 diabetes mellitus (T2DM). However, the extensive pharmacological characteristics and the underlying mechanism are unknown. This study investigated the mechanisms by which SZ-A ameliorates glucose metabolism in KKAy mice, an animal model of T2DM. Diabetic KKAy mice were treated intragastrically with SZ-A once daily for 8 weeks, after which glucose levels, lipid metabolism, gut microbiome, systemic inflammatory factors, luminal concentrations of short-chain fatty acids (fecal samples), and ileal proteomic changes were evaluated. The ileum tissues were collected, and the effects of SZ-A on pathological inflammatory damage were evaluated by hematoxylin and eosin staining, immunofluorescence, and immunohistochemistry. The mRNA and protein expression levels of various inflammatory markers, including monocyte chemoattractant protein-1 and phosphorylated nuclear factor kappa B p65, were detected in the ileum tissues. SZ-A improved glucose metabolism with enhanced insulin response and elevated glucagon-like peptide 1 (GLP-1) nearly 2.7-fold during the glucose tolerance test in diabetic KKAy mice. Gut microbiota analysis demonstrated that SZ-A administration elevated the abundance of Bacteroidaceae and Verrucomicrobia, reduced the levels of Rikenellaceae and Desulfovibrionaceae; and increased the concentrations of fecal acetic and propionic acids compared to the diabetic model group. Additionally, SZ-A markedly improved ileal inflammatory injury and pro-inflammatory macrophage infiltration and improved intestinal mucosal barrier function in diabetic KKAy mice. SZ-A also attenuated the levels of circulating endotoxin, pro-inflammatory cytokines, and chemokines in the mice sera. Collectively, SZ-A ameliorated the overall metabolic profile including glucose and lipid metabolism in KKAy mice, which may be associated with an improvement in GLP-1 and insulin secretion, at least in part by modulating the gut microbiome and relieving the degree of ileal and systemic inflammation.

scholarly journals Bugs, genes, fatty acids, and serotonin: Unraveling inflammatory bowel disease?

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1146 ◽  
Author(s):  
Jonathan D. Kaunitz ◽  
Piyush Nayyar
Keyword(s):  
Fatty Acids ◽  
Short Chain Fatty Acids ◽  
Intestinal Microbiome ◽  
Mucosal Barrier ◽  
Neural Systems ◽  
Integrative Approach ◽  
Mucosal Barrier Function ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Glucagon Like Peptide

The annual incidence of the inflammatory bowel diseases (IBDs) ulcerative colitis and Crohn’s disease has increased at an alarming rate. Although the specific pathophysiology underlying IBD continues to be elusive, it is hypothesized that IBD results from an aberrant and persistent immune response directed against microbes or their products in the gut, facilitated by the genetic susceptibility of the host and intrinsic alterations in mucosal barrier function. In this review, we will describe advances in the understanding of how the interaction of host genetics and the intestinal microbiome contribute to the pathogenesis of IBD, with a focus on bacterial metabolites such as short chain fatty acids (SCFAs) as possible key signaling molecules.  In particular, we will describe alterations of the intestinal microbiota in IBD, focusing on how genetic loci affect the gut microbial phylogenetic distribution and the production of their major microbial metabolic product, SCFAs. We then describe how enteroendocrine cells and myenteric nerves express SCFA receptors that integrate networks such as the cholinergic and serotonergic neural systems and the glucagon-like peptide hormonal pathway, to modulate gut inflammation, permeability, and growth as part of an integrated model of IBD pathogenesis.  Through this integrative approach, we hope that novel hypotheses will emerge that will be tested in reductionist, hypothesis-driven studies in order to examine the interrelationship of these systems in the hope of better understanding IBD pathogenesis and to inform novel therapies.

scholarly journals N-Acetyl Serotonin Alleviates Oxidative Damage by Activating Nuclear Factor Erythroid 2-Related Factor 2 Signaling in Porcine Enterocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 303
Author(s):  
Haiwei Liang ◽  
Ning Liu ◽  
Renjie Wang ◽  
Yunchang Zhang ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastrointestinal Diseases ◽  
Mucosal Barrier ◽  
Related Factor ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Downstream Target ◽  
Underlying Mechanisms ◽  
And Function

Apoptosis of intestinal epithelial cells following oxidative stress is a major cause of mucosal barrier dysfunction and is associated with the pathogenesis of various gastrointestinal diseases. Although L-tryptophan (Trp) is known to improve intestinal integrity and function, a beneficial effect of N-acetyl serotonin (NAS), a metabolite of Trp, on the apoptosis of enterocytes and the underlying mechanisms remain largely unknown. In the present study, we showed that porcine enterocytes treated with 4-hydroxy-2-nonenal (4-HNE), a metabolite of lipid peroxidation, led to upregulation of apoptotic proteins, including Bax and cleaved caspase-3, and reduction of tight junction proteins. These effects of 4-HNE were significantly abrogated by NAS. In addition, NAS reduced ROS accumulation while increasing the intracellular concentration of glutathione (GSH), and the abundance of the Nrf2 protein in the nucleus and its downstream target proteins. Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Taken together, we demonstrated that NAS attenuated oxidative stress-induced cellular injury in porcine enterocytes by regulating Nrf2 signaling. These findings provide new insights into a functional role of NAS in maintaining intestinal homeostasis.

FC 083PROBIOTIC L.CASEI ZHANG  SLOWS THE PROGRESSION OF ACUTE AND CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Rui Zeng
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ischemia Reperfusion ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
Health Concern ◽  
Mucosal Barrier ◽  
Protective Effects ◽  
Mucosal Barrier Function ◽  
Probiotic Lactobacillus

Abstract Background and Aims The relationship between gut microbial dysbiosis and acute or chronic kidney disease is currently acknowledged to be a health concern which is characterized by immune dysregulation and metabolic disorder. However, the therapeutic strategies remain to be developed. In the present study, we examined the protective effects and mechanisms of action of probiotic Lactobacillus casei Zhang (L. casei Zhang) on bilateral renal ischemia-reperfusion (I/R)-induced injury in mice. Method We orally gavaged male C57BL/6 mice with or without L. casei Zhang and probiotic Lactobacillus acidophilus (L. acidophilus) for 4 weeks (1 × 109 CFU per day) prior to being subjected to ischemia-reperfusion (I/R)-induced injury. Serum, colons and renal samples were collected after 5 days and 28 days. The composition and abundance of gut microbiota was investigated by using 16S rRNA. LC-MS metabolomic analysis technology and GC-MS analysis technology were used to investigate the metabolic alterations. To define the intra-renal cell subsets that are involved in L. casei Zhang-induced renoprotection, we performed single-cell RNA-sequencing (scRNA-seq) of kidney samples dissected from L. casei Zhang pretreated mice at day 5 after I/R along with samples from non-treated controls. Results Compared to L.acidophilus, L. casei Zhang demonstrated superior capacity in restoring intestinal flora homeostasis, protecting intestinal mucosal barrier function and improving the disrupted metabolomic profile. L. casei Zhang not only elevated the short chain fatty acids (SCFAs) in serum and kidney, but also significantly increased nicotinamide, by which L. casei Zhang inhibited renal inflammatory response and alleviated the damage of renal tubular epithelial cells (TECs) via interacting with SCFAs receptors on macrophages and TECs, and activating NAD+ metabolism in injured kidneys. Conclusion These results show that oral administration of L. casei Zhang, by altering SCFAs and nicotinamide metabolism, is a potential therapy to mitigate kidney injury and slow the progression of renal decline.

scholarly journals Modification of Immunological Parameters, Oxidative Stress Markers, Mood Symptoms, and Well-Being Status in CFS Patients after Probiotic Intake: Observations from a Pilot Study

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Letizia Venturini ◽  
Sara Bacchi ◽  
Enrica Capelli ◽  
Lorenzo Lorusso ◽  
Giovanni Ricevuti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune System ◽  
Bacterial Species ◽  
Preliminary Investigation ◽  
Well Being ◽  
Chronic Fatigue ◽  
Mucosal Barrier ◽  
Low Grade ◽  
Immunological Parameters ◽  
Mucosal Barrier Function

The present study discusses about the effects of a combination of probiotics able to stimulate the immune system of patients affected by Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). To this purpose, patients diagnosed according to Fukuda’s criteria and treated with probiotics were analyzed by means of clinical and laboratory evaluations, before and after probiotic administrations. Probiotics were selected considering the possible pathogenic mechanisms of ME/CFS syndrome, which has been associated with an impaired immune response, dysregulation of Th1/Th2 ratio, and high oxidative stress with exhaustion of antioxidant reserve due to severe mitochondrial dysfunction. Immune and oxidative dysfunction could be related with the gastrointestinal (GI) chronic low-grade inflammation in the lamina propria and intestinal mucosal surface associated with dysbiosis, leaky gut, bacterial translocation, and immune and oxidative dysfunction. Literature data demonstrate that bacterial species are able to modulate the functions of the immune and oxidative systems and that the administration of some probiotics can improve mucosal barrier function, modulating the release of proinflammatory cytokines, in CFS/ME patients. This study represents a preliminary investigation to verifying the safety and efficacy of a certain combination of probiotics in CFS/ME patients. The results suggest that probiotics can modify the well-being status as well as inflammatory and oxidative indexes in CFS/ME patients. No adverse effects were observed except for one patient, which displayed a flare-up of symptoms, although all inflammatory parameters (i.e., cytokines, fecal calprotectin, ESR, and immunoglobulins) were reduced after probiotic intake. The reactivation of fatigue symptoms in this patient, whose clinical history reported the onset of CFS/ME following mononucleosis, could be related to an abnormal stimulation of the immune system as suggested by a recent study describing an exaggerated immune activation associated with chronic fatigue.

scholarly journals Select Polyphenol-Rich Berry Consumption to Defer or Deter Diabetes and Diabetes-Related Complications

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2538
Author(s):  
Ahsan Hameed ◽  
Mauro Galli ◽  
Edyta Adamska-Patruno ◽  
Adam Krętowski ◽  
Michal Ciborowski
Keyword(s):  
Oxidative Stress ◽  
Short Chain Fatty Acids ◽  
Clinical Findings ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Human Diet ◽  
Markers Of Oxidative Stress ◽  
Healthy Obese ◽  
Berry Extracts

Berries are considered “promising functional fruits” due to their distinct and ubiquitous therapeutic contents of anthocyanins, proanthocyanidins, phenolic acids, flavonoids, flavanols, alkaloids, polysaccharides, hydroxycinnamic, ellagic acid derivatives, and organic acids. These polyphenols are part of berries and the human diet, and evidence suggests that their intake is associated with a reduced risk or the reversal of metabolic pathophysiologies related to diabetes, obesity, oxidative stress, inflammation, and hypertension. This work reviewed and summarized both clinical and non-clinical findings that the consumption of berries, berry extracts, purified compounds, juices, jams, jellies, and other berry byproducts aided in the prevention and or otherwise management of type 2 diabetes mellitus (T2DM) and related complications. The integration of berries and berries-derived byproducts into high-carbohydrate (HCD) and high-fat (HFD) diets, also reversed/reduced the HCD/HFD-induced alterations in glucose metabolism-related pathways, and markers of oxidative stress, inflammation, and lipid oxidation in healthy/obese/diabetic subjects. The berry polyphenols also modulate the intestinal microflora ecology by opposing the diabetic and obesity rendered symbolic reduction of Bacteroidetes/Firmicutes ratio, intestinal mucosal barrier dysfunction-restoring bacteria, short-chain fatty acids, and organic acid producing microflora. All studies proposed a number of potential mechanisms of action of respective berry bioactive compounds, although further mechanistic and molecular studies are warranted. The metabolic profiling of each berry is also included to provide up-to-date information regarding the potential anti-oxidative/antidiabetic constituents of each berry.

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