Psyllium fiber improves hangovers and inflammatory liver injury by inhibiting intestinal drinking
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ABSTRACT:
SUBMITTER: Yang K
PROVIDER: S-EPMC11239518 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:The aim of the study was to determine the influence of the different shares (0/100, 5/95, 10/90 and 15/85 ratios) of a ground psyllium fiber (PF) mixture of 80% psyllium seeds (Plantago psyllium) and 20% psyllium husk (Plantago ovata Forsk) on the quality characteristics, chemical composition, total polyphenolic content (TPC), and antioxidant activity of rye bread (RB). The study was conducted with rye flour (RF) type 580 and 720 and two dough preparation methods (single-phase-1F, two-phase-2F). The inclusion of psyllium fiber in rye bread resulted in an increase in the overbaking of bread by 12.4%, total protein by 1.7%, ash by almost twofold, and TDF content by more than twofold. Psyllium fiber addition also led to a twofold improvement in antioxidant activity and an increase in TPC from 35.5 to 109.1 mg GAE/100 g d.m., as well as enhanced porosity of the crumb from 7.1 to 7.6 points on the Mohs scale. However, it caused a decrease in specific loaf volume by 10%, springiness by 3.5%, chewiness by almost 12%, and gumminess of the crumb by 8.1%. A darkening of the crust (reduction in the L* value by 10.7%) and crumb (reduction in the L* value by 37.6%) was observed as well. Notably, the results indicated that a 10% share of PF can be considered a potentially beneficial and functional ingredient, promoting health benefits without negatively affecting the physical and sensory qualities of rye bread. This suggests the potential use of PF for enhancing the nutritional value of RB without compromising its overall quality.
| S-EPMC10572817 | biostudies-literature
Project description:Intestinal barrier function defects and dysregulation of intestinal immune responses are two key contributory factors in the pathogenesis of ulcerative colitis (UC). Phenazine biosynthesis-like domain-containing protein (PBLD) was recently identified as a tumor suppressor in gastric cancer, hepatocellular carcinoma, and breast cancer; however, its role in UC remains unclear. Therefore, we analyzed colonic tissue samples from patients with UC and constructed specific intestinal epithelial PBLD-deficient (PBLDIEC-/-) mice to investigate the role of this protein in UC pathogenesis. We found that epithelial PBLD was decreased in patients with UC and was correlated with levels of tight junction (TJ) and inflammatory proteins. PBLDIEC-/- mice were more susceptible to dextran sulfate sodium (DSS)- and 2,4,6-trinitrobenzene sulfonic acid-induced colitis compared with wild-type (WT) mice. In DSS-induced colitis, PBLDIEC-/- mice had impaired intestinal barrier function and greater immune cell infiltration in colonic tissue than WT mice. Furthermore, TJ proteins were markedly reduced in PBLDIEC-/- mice compared with WT mice with colitis. Nuclear factor (NF)-κB activation was markedly elevated and resulted in higher expression levels of downstream effectors (C-C motif chemokine ligand 20, interleukin [IL]-1β, IL-6, and tumor necrosis factor [TNF]-α) in colonic epithelial cells isolated from PBLDIEC-/- mice than WT mice with colitis. PBLD overexpression in intestinal epithelial cells (IECs) consistently inhibited TNF-α/interferon-γ-induced intestinal barrier disruption and TNF-α-induced inflammatory responses via the suppression of NF-κB. In addition, IKK inhibition (IKK-16) rescued excessive inflammatory responses induced by TNF-α in PBLD knockdown FHC cells. Co-immunoprecipitation assays showed that PBLD may interact with IKKα and IKKβ, thus inhibiting NF-κB signaling, decreasing inflammatory mediator production, attenuating colonic inflammation, and improving intestinal barrier function. Modulating PBLD expression may provide a novel approach for treatment in patients with UC.
| S-EPMC8166876 | biostudies-literature
Project description:Recent evidence supports a significant association between the intake of dietary fiber and levels of inflammatory markers. The objective of this study was to determine whether daily fiber supplementation would reduce levels of inflammatory markers.This study was a prospective randomized controlled trial at a single university medical center. Participants were overweight or obese adults with no history of heart disease. The intervention was psyllium supplementation at either 7 or 14 g/d for 3 months compared with no supplements in a control group. The main outcome measure was change in level of high-sensitivity C-reactive protein (hsCRP) concentration; secondary outcomes included changes in interleukin-6 (IL-6) levels, fibrinogen levels, and white blood cell (WBC) count. Protocol completers attended at least 2 visits and took more than 75% of the prescribed fiber dose.In this intent-to-treat analysis (n = 158), there were no significant differences between either of the 2 treatment groups and the control group in the amount of change in CRP, fibrinogen, or IL-6 levels or in WBC count (P>.05). In the analysis of protocol completers (n = 132), there also were no significant differences between the groups except for a small decrease in fibrinogen level in the high-fiber group (-6 mg/dL [-0.18 micromol/L] compared with 13 mg/dL [0.38 micromol/L] in the control group, P<.05).Psyllium fiber supplementation did not significantly reduce CRP levels in overweight or obese individuals in this trial, and changes in other markers were not consistent. Further research is needed to determine whether other fibers or nutrients can reduce inflammatory markers.
| S-EPMC2267421 | biostudies-literature
Project description:Gardenia jasminoides Ellis, which belongs to the Rubiaceae family, is a widely used traditional Chinese medicine. Although effect of Gardenia jasminoides Ellis has been widely reported, its anti-inflammatory role in intestinal mucosal injury induced by LPS remains unclear. In the present study, we investigated the effects of decoction extracted from Gardenia jasminoides on the morphology and intestinal antioxidant capacity of duodenum induced by LPS in mice. Further analysis was carried out in the expression of inflammatory and anti-inflammatory cytokines. Nuclear factor-kappa B (NF-κB) was determined by Western blot. Gardenia jasminoides water extract was qualitative analyzed by high-performance liquid chromatography coupled with electro spray ionization quadrupole time-of-flight mass spectrometry. The results showed that Gardenia decoction markedly inhibited the LPS-induced Tumor necrosis factor (TNF)-α, Interleukin (IL)-6, IL-8, and IL-1 production. It was also observed that Gardenia decoction attenuated duodenum histopathology changes in the mouse models. Furthermore, Gardenia decoction inhibited the expression of NF-κB in LPS stimulated mouse duodenum. These results suggest that Gardenia decoction exerts an anti-inflammatory and antioxidant property by up-regulating the activities of the total antioxidant capacity (T-AOC), the total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px). Gardenia decoction is highly effective in inhibiting intestinal mucosal damage and may be a promising potential therapeutic reagent for intestinal mucosal damage treatment.
| S-EPMC6447716 | biostudies-other
Project description:Feeding dietary fiber is known to provide us many beneficial effects. We used microarrays to detail the changes of gene expression in colons of mice fed the psyllium fiber for 5 days.
2017-05-26 | GSE99292 | GEO
Project description:Hepatic sinusoidal obstruction syndrome (HSOS) is a rare liver disease with considerable morbidity and mortality. (-)-Epicatechin (EPI) is a natural flavonol. This study aims to investigate the protection of EPI against monocrotaline (MCT)-induced HSOS and its engaged mechanism. Results of serum alanine/aspartate aminotransferases (ALT/AST) activities, total bilirubin (TBil) and bile acids (TBA) amounts, liver histological evaluation, scanning electron microscope observation and hepatic metalloproteinase-9 (MMP-9) expression all demonstrated the protection by EPI against MCT-induced HSOS in rats. EPI attenuated liver oxidative injury induced by MCT. EPI enhanced the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased the expression of its downstream antioxidant genes in rats. Molecular docking results implied the potential interaction of EPI with the Nrf2 binding site in kelch-like ECH-associated protein-1 (Keap1). The EPI-provided protection against MCT-induced HSOS was diminished in Nrf2 knock-out mice when mice were treated with MCT for 24 h but not for 48 h. However, EPI reduced the increased liver myeloperoxidase (MPO) activity, hepatic infiltration of immune cells, pro-inflammatory cytokines expression and nuclear factor κB (NFκB) activation in both wild-type and Nrf2 knock-out mice when mice were treated with MCT for 48 h. EPI reduced the elevated serum heat shock protein 60 (HSP60) content, and reversed the decreased mitochondria expression of HSP60 and Lon in livers from MCT-treated rats. Furthermore, the MCT-induced HSOS was markedly alleviated in mice treated with anti-HSP60 antibody. Taken together, this study demonstrates that EPI attenuates MCT-induced HSOS by reducing liver oxidative injury via activating Nrf2 antioxidant pathway and inhibiting liver inflammatory injury through abrogating NFκB signaling pathway initiated by HSP60.
| S-EPMC6395886 | biostudies-literature
Project description:Liver-resident macrophages (Kupffer cells, KCs) and autophagy play critical roles in the pathogenesis of toxin-induced liver injury. Recent evidence indicates that autophagy can regulate macrophage M1/M2 polarization under different inflammatory conditions. Polyamines, including putrescine, spermidine, and spermine (SPM), are polycations with anti-oxidative, anti-aging, and cell autophagy induction properties. This study aimed to determine the mechanisms by which SPM protects against thioacetamide (TAA)-induced acute liver injury in a mouse model. Pretreatment with SPM significantly alleviated liver injury and reduced intrahepatic inflammation in TAA-induced liver injury compared to controls. SPM markedly inhibited M1 polarization, but promoted M2 polarization of KCs obtained from TAA-exposed livers, as evidenced by decreased IL-1β and iNOS gene induction but increased Arg-1 and Mrc-1 gene induction accompanied by decreased STAT1 activation and increased STAT6 activation. Furthermore, pretreatment with SPM enhanced autophagy, as revealed by increased LC3B-II levels, decreased p62 protein expression, and increased ATG5 protein expression in TAA-treated KCs. Knockdown of ATG5 in SPM-pretreated KCs by siRNA resulted in a significant increase in pro-inflammatory TNF-α and IL-6 secretion and decreased anti-inflammatory IL-10 secretion after TAA treatment, while no significant changes were observed in cytokine production in the TAA treatment alone. Additionally, the effect of SPM on regulation of KC M1/M2 polarization was abolished by ATG5 knockdown in TAA-exposed KCs. Finally, in vivo ATG5 knockdown in KCs abrogated the protective effect of SPM against TAA-induced acute liver injury. Our results indicate that SPM-mediated autophagy inhibits M1 polarization, while promoting M2 polarization of KCs in TAA-treated livers via upregulation of ATG5 expression, leading to attenuated liver injury. This study provides a novel target for the prevention of acute liver injury.
| S-EPMC5940752 | biostudies-literature
Project description:Puerarin, an isoflavone component extracted from herb radix puerariae, is widely used in China in the treatment of immune diseases and inflammation. Previous studies have demonstrated that puerarin prevented acute lung injury by regulating inflammatory responses. However, the effect of puerarin on acute liver injury (ALI) was unclear. The purpose of this study was to explore the beneficial effects of puerarin when applied to ALI. We found that puerarin inhibited liver injury and inflammatory cell infiltration in lipopolysaccharide (LPS)/D-galactose (D-Gal)-induced acute liver failure and the liver pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) in liver tissues with ALI and LPS-induced L-02 cells but upregulated the expression level of zinc finger E-box-binding homeobox 2 (ZEB2). Significantly, the results of this study showed that the inhibition of liver pro-inflammatory cytokine (IL-1β, IL-6, and TNF-α) production in LPS-induced L-02 cells was caused by ZEB2 overexpression. However, knocking down ZEB2 promoted LPS-mediated secretion of liver pro-inflammatory cytokines in L-02 cells. Additional experiments showed that puerarin inhibited the activation of the NF-κB signaling pathway by elevating ZEB2 expression in L-02 cells. In summary, puerarin most likely prevented activation of the pro-inflammatory factors and reduced LPS/D-Gal-induced liver injury by enhancing the ZEB2 expression level and, consequently, blocking activation of the NF-κB signaling pathway in the liver.
| S-EPMC8378253 | biostudies-literature
Project description:The E3 ubiquitin ligase RING finger protein 115 (RNF115), also known as breast cancer-associated gene 2 (BCA2), has been linked with the growth of some cancers and immune regulation, which is negatively correlated with prognosis. Here, it is demonstrated that the RNF115 deletion can protect mice from acute liver injury (ALI) induced by the treatment of lipopolysaccharide (LPS)/D-galactosamine (D-GalN), as evidenced by decreased levels of alanine aminotransaminase, aspartate transaminase, inflammatory cytokines (e.g., tumor necrosis factor α and interleukin-6), chemokines (e.g., MCP1/CCL2) and inflammatory cell (e.g., monocytes and neutrophils) infiltration. Moreover, it was found that the autophagy activity in Rnf115-/- livers was increased, which resulted in the removal of damaged mitochondria and hepatocyte apoptosis. However, the administration of adeno-associated virus Rnf115 or autophagy inhibitor 3-MA impaired autophagy and aggravated liver injury in Rnf115-/- mice with ALI. Further experiments proved that RNF115 interacts with LC3B, downregulates LC3B protein levels and cell autophagy. Additionally, Rnf115 deletion inhibited M1 type macrophage activation via NF-κB and Jnk signaling pathways. Elimination of macrophages narrowed the difference in liver damage between Rnf115+/+ and Rnf115-/- mice, indicating that macrophages were linked in the ALI induced by LPS/D-GalN. Collectively, for the first time, we have proved that Rnf115 inactivation ameliorated LPS/D-GalN-induced ALI in mice by promoting autophagy and attenuating inflammatory responses. This study provides new evidence for the involvement of autophagy mechanisms in the protection against acute liver injury.
| S-EPMC10739886 | biostudies-literature
Project description:The phenomenon of intestinal dysfunction is widely observed in white shrimp (Litopenaeus vannamei) culture, and β-1,3-glucan has been confirmed to be beneficial in intestinal health with a lack understanding of its underlying mechanism. Proteobacteria, Firmicutes, and Actinobacteria served as the predominant phyla inhabiting the intestine of white shrimp, whilst a significant variation in their proportion was recorded in shrimp fed with basal and β-1,3-glucan supplementation diets in this study. Dietary supplementation of β-1,3-glucan could dramatically increase the microbial diversity and affect microbial composition, concurrent with a notable reduction in the ratio of opportunistic pathogen Aeromonas, gram-negative microbes, from Gammaproteobacteria compared to the basal diet group. The benefits for microbial diversity and composition by β-1,3-glucan improved the homeostasis of intestinal microbiota through the increase of specialists’ number and inhibition of microbial competition caused by Aeromonas in ecological networks; afterward, the inhibition of Aeromonas by β-1,3-glucan diet dramatically suppressed microbial metabolism related to lipopolysaccharide biosynthesis, followed by a conspicuous decrease in the intestinal inflammatory response. The improvement of intestinal health referred to the elevation in intestinal immune and antioxidant capacity, ultimately contributing to the growth of shrimp fed β-1,3-glucan. These results suggested that β-1,3-glucan supplementation improved the intestinal health of white shrimp through the modulation of intestinal microbiota homeostasis, the suppression of intestinal inflammatory response, and the elevation of immune and antioxidant capacity, and subsequently promoted the growth of white shrimp.
| S-EPMC9922984 | biostudies-literature