scholarly journals Resveratrol Alleviates Oxidative Stress Induced by Oxidized Soybean Oils and Improves Gut Function via Changing Gut Microbiota in Weaned Piglets

2022 ◽  
Author(s):  
Yanan Gao ◽  
Qingwei Meng ◽  
Xin Song ◽  
Qianqian Zhao ◽  
Baoming Shi
Keyword(s):  
Acetic Acid ◽  
Gut Microbiota ◽  
Digestive Enzyme ◽  
Intestinal Barrier ◽  
Redox Status ◽  
Weaned Piglets ◽  
Soybean Oils ◽  
Tnf Α ◽  
Similar Body ◽  
Α Level

Abstract Background: The objective of this study was to investigate the effects of dietary resveratrol supplementation on growth performance, redox status, inflammatory state, and intestinal function of weaned piglets fed oxidized soybean oils.Methods: A total of twenty-eight castrated weaned male piglets with a similar body weight of 10.19 ±1 kg were randomly assigned to 4 dietary treatments for 28 days feeding trial with 7 replications per treatment and 1 piglet per replicate. Treatments were arranged as a 2×2 factorial with oil type [fresh soybean oils (FSOs) vs. oxidized soybean oils (OSOs)] and dietary resveratrol (RES) (0 vs. 300 mg/kg).Result: Inclusion of OSOs decreased the villus/crypt ratio (VCR), while the villus height (VH) and VCR in the jejunum of weaned piglets was increased by dietary RES (P< 0.05). The activities of lipase, chymotrypsin, and lactase were decreased by OSOs, however dietary RES supplementation increased the activities of lipase, chymotrypsin, lactase, and α-amylase in the jejunum of weaned piglets (P< 0.05). Dietary RES increased the apparent digestibility of crude fat (EE). Dietary RES supplementation in the diets supplemented with OSOs decreased the level of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) in the plasma of weaned piglets, but failed to influence the IL-1β, IL-6, IL-8, and TNF-α level when diets supplemented with FSOs. Dietary RES alleviated the decrease of total-superoxide dismutase activity in the plasma of weaned piglets fed OSOs (P< 0.05). Dietary supplemented with OSOs and RES decreased the level of H2O2 in the plasma of weaned piglets (P< 0.05). RES alleviates the intestinal barrier damage fed OSOs in weaned piglets by increasing the mRNA expression of ZO-1 and Occludin. It is noteworthy that inclusion of OSOs in diets increased the abundance of Actinobacteria, and decreased the abundance of Tenercutes (P< 0.05). RES increased the abundance of Firmicutes, and decreased the abundance of Bacteroidetes (P< 0.05). At the genus level, RES decreased the abundance of Prevotella-1, Prevotellaceae UCG003, and Clostridium_sensu_stricto_6 in the colon. OSOs decreased the level of acetic acid, and dietary RES increased the level of acetic acid and butyric acid in the colon of weaned piglets.Conclusions: Dietary RES supplementation improved the villus-crypt structure, digestive enzyme activities and alleviated OSOs induced digestive absorption disorder. In addition, RES may alleviate OSOs immune status and energy metabolism of weaned piglets by affecting gut microbiota and its metabolite SCFAs. Notably, this positive effect of RES on OSOs may be related to decrease in the abundance of Prevotella_1 and Prevotellaceae_UCG-003.

scholarly journals Association of Hyperuricemia With Immune Disorders and Intestinal Barrier Dysfunction

2020 ◽  
Vol 11 ◽  
Author(s):  
Qiulan Lv ◽  
Daxing Xu ◽  
Xuezhi Zhang ◽  
Xiaomin Yang ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Uric Acid ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Urate Oxidase ◽  
Intestinal Immunity ◽  
Immune Disorders ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Gut Barrier Function ◽  
Tnf Α

BackgroundMore than 30–40% of uric acid is excreted via the intestine, and the dysfunction of intestinal epithelium disrupts uric acid excretion. The involvement of gut microbiota in hyperuricemia has been reported in previous studies, but the changes and mechanisms of intestinal immunity in hyperuricemia are still unknown.MethodsThis study developed a urate oxidase (Uox)-knockout (Uox–/–) mouse model for hyperuricemia using CRISPR/Cas9 technology. The lipometabolism was assessed by measuring changes in biochemical indicators. Furthermore, 4-kDa fluorescein isothiocyanate–labeled dextran was used to assess gut barrier function. Also, 16S rRNA sequencing was performed to examine the changes in gut microbiota in mouse feces. RNA sequencing, Western blot, Q-PCR, ELISA, and immunohistochemical analysis were used for measuring gene transcription, the number of immune cells, and the levels of cytokines in intestinal tissues, serum, kidney, liver, pancreas, and vascellum.ResultsThis study showed that the abundance of inflammation-related microbiota increased in hyperuricemic mice. The microbial pattern recognition–associated Toll-like receptor pathway and inflammation-associated TNF and NF-kappa B signaling pathways were significantly enriched. The increased abundance of inflammation-related microbiota resulted in immune disorders and intestinal barrier dysfunction by upregulating TLR2/4/5 and promoting the release of IL-1β and TNF-α. The levels of epithelial tight junction proteins occludin and claudin-1 decreased. The expression of the pro-apoptotic gene Bax increased. The levels of LPS and TNF-α in systemic circulation increased in hyperuricemic mice. A positive correlation was observed between the increase in intestinal permeability and serum levels of uric acid.ConclusionHyperuricemia was characterized by dysregulated intestinal immunity, compromised intestinal barrier, and systemic inflammation. These findings might serve as a basis for future novel therapeutic interventions for hyperuricemia.

scholarly journals Transcriptome Analysis of Intestinal Dysfunction in Newborn Piglets with Intrauterine Growth Restriction and Improve their Performance by Dimethylglycine Sodium Salt Supplementation after Weaning

2021 ◽  
Author(s):  
Kaiwen Bai ◽  
Luyi Jiang ◽  
Qiming Li ◽  
Jingfei Zhang ◽  
Lili Zhang ◽  
...  
Keyword(s):  
Sodium Salt ◽  
Mitochondrial Function ◽  
Intrauterine Growth Restriction ◽  
Digestive Enzyme ◽  
Redox Status ◽  
Growth Restriction ◽  
Rna Seq ◽  
Weaned Piglets ◽  
Intrauterine Growth ◽  
Newborn Piglets

Abstract Background Few studies are available on the mechanism of intestinal dysfunction in newborn piglets with intrauterine growth restriction (IUGR). This work aimed to study the mechanism of jejunum dysfunction in IUGR newborn piglets through RNA-seq and improve their performance by dimethylglycine sodium salt (DMG-Na) supplementation after weaning. Methods In total, 13 normal birth weight (NBW) newborn piglets and 23 IUGR newborn piglets were obtained. Among them, 3 NBW and 3 IUGR newborn piglets were selected and stunned by electric shock after birth without suckling and collected the jejunum samples for RNA-sEq. After weaning at 21 days, they were randomly assigned to 3 groups (n = 10): NBW weaned piglets fed with common basal diets (N); IUGR weaned piglets fed with common basal diets (I); IUGR weaned piglets fed with common basal diets plus 0.1% DMG-Na (ID). All piglets are slaughtered at 49 days of age to collect serum and jejunum samples. Results The hub genes, including ATP8, C11orf86, CDKN1C, DDX58. HPX, INHBB, LECT2, ND1, NFIX, PRDM5, PSD3, SCD, and ZNF770, were found from the data analyzed by RNA-seq and WGCNA. Interestingly, we found ATP8 was the most significantly changed gene, which was crucial in maintaining mitochondrial function. After weaning, the growth performance of ID group was improved (P < 0.05) compared to that in I group. Jejunum histological morphology and its sub-organelle ultrastructure, serum immunoglobulin, jejunum sIgA level, and jejunum digestive enzyme activity were improved (P < 0.05) in ID group compared to those in I group. The redox status of serum, jejunum and its mitochondrial, as well as jejunum redox status-related and mitochondrial function-related gene expression level and protein content were improved (P < 0.05) in ID group in comparison to those in I group. Conclusion The activity of the SIRT1/PGC1α pathway was inhibited in the IUGR weaned piglets, which in turn leads to damage to their redox status and jejunum structure and function, and finally lowers their performance. The IUGR weaned piglets activate the SIRT1/PGC1α pathway by taking in the antioxidant substance like DMG-Na, thereby improving their unfavorable body state.

Bilberry anthocyanin extract promotes intestinal barrier function and inhibits digestive enzyme activity by regulating the gut microbiota in aging rats

2019 ◽  
Vol 10 (1) ◽  
pp. 333-343 ◽  
Author(s):  
Jing Li ◽  
Tao Wu ◽  
Na Li ◽  
Xuening Wang ◽  
Guiyun Chen ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Gut Microbiota ◽  
Barrier Function ◽  
Digestive Enzyme ◽  
Intestinal Barrier ◽  
Digestive Enzyme Activity ◽  
Intestinal Barrier Function ◽  
Aging Rats

Bilberry anthocyanin extract promotes intestinal barrier function and inhibits digestive enzyme activity through regulating the gut microbiota in aging rats.

scholarly journals Lactobacillus acidophilus Exerts Neuroprotective Effects in Mice with Traumatic Brain Injury

2019 ◽  
Vol 149 (9) ◽  
pp. 1543-1552 ◽  
Author(s):  
Yuanyuan Ma ◽  
Tianyao Liu ◽  
Jingjing Fu ◽  
Shaoli Fu ◽  
Chen Hu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gut Microbiota ◽  
Lactobacillus Acidophilus ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Microbiota Composition ◽  
Neuroprotective Effects ◽  
Tnf Α ◽  
Underlying Mechanisms

ABSTRACT Background Traumatic brain injury (TBI) causes dysbiosis and intestinal barrier disruption, which further exacerbate brain damage via an inflammatory pathway. Gut microbiota remodeling by Lactobacillus acidophilus (LA) is a potential intervention. Objective The aim of this study was to investigate the neuroprotective effects of LA in TBI and elucidated underlying mechanisms. Methods C57BL/6 male mice (aged 8–9 wk) were subjected to weight-drop impact and gavaged with saline (TBI + vehicle) or LA (1 × 1010 CFU) (TBI + LA) on the day of injury and each day after for 1, 3, or 7 d. The sham + vehicle mice underwent craniotomy without brain injury and were gavaged with saline. Sensorimotor functions were determined pre-TBI and 1, 3, and 7 d postinjury. Indexes of neuroinflammation, peripheral inflammation, and intestinal barrier function were measured on days 3 and 7. Microbiota composition was measured 3 d postinjury. The data were mainly analyzed by 2-factor ANOVA. Results Compared with sham + vehicle mice, the TBI + vehicle mice exhibited impairments in the neurological severity score (+692%, day 3; +600%, day 7) and rotarod test (−58%, day 3; −45%, day 7) (P < 0.05), which were rescued by LA. The numbers of microglia (total and activated) and astrocytes and concentrations of TNF-α and IL1-β in the perilesional cortex were elevated in the TBI + vehicle mice on day 3 or 7 compared with sham + vehicle mice (P < 0.05) and were normalized by LA. Compared with sham + vehicle mice, the TBI + vehicle mice exhibited increased serum concentrations of endotoxin and TNF-α, and intestinal barrier permeability (D-lactate) on days 3 and 7 (P < 0.05), and these changes were alleviated by LA. Three days postinjury, the microbiota composition was disrupted in the TBI + vehicle mice compared with sham + vehicle mice (P < 0.05), which was restored by LA. Conclusion Our results demonstrate that LA exerts neuroprotective effects that may be associated with gut microbiota remodeling in TBI mice.

scholarly journals Prevotellaceae produces butyrate to alleviate PD-1/PD-L1 inhibitor-related cardiotoxicity via PPARα-CYP4X1 axis in colonic macrophages

2022 ◽  
Vol 41 (1) ◽  
Author(s):  
Yaxin Chen ◽  
Yanzhuo Liu ◽  
Yang Wang ◽  
Xuewei Chen ◽  
Chenlong Wang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Gut Microbiota ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitor ◽  
Checkpoint Inhibitor ◽  
Intestinal Barrier ◽  
Cardiomyocyte Apoptosis ◽  
Tnf Α ◽  
Gut Microbiota Dysbiosis ◽  
Proinflammatory Factors

Abstract Background Immune checkpoint inhibitor-related cardiotoxicity is one of the most lethal adverse effects, and thus, the identification of underlying mechanisms for developing strategies to overcome it has clinical importance. This study aimed to investigate whether microbiota-host interactions contribute to PD-1/PD-L1 inhibitor-related cardiotoxicity. Methods A mouse model of immune checkpoint inhibitor-related cardiotoxicity was constructed by PD-1/PD-L1 inhibitor BMS-1 (5 and 10 mg/kg), and cardiomyocyte apoptosis and cardiotoxicity were determined by hematoxylin and eosin, Masson’s trichome and TUNEL assays. 16S rRNA sequencing was used to define the gut microbiota composition. Gut microbiota metabolites short-chain fatty acids (SCFAs) were determined by HPLC. The serum levels of myocardial enzymes (creatine kinase, aspartate transaminase, creatine kinase-MB and lactate dehydrogenase) and the production of M1 factors (TNF-α and IL-1β) were measured by ELISA. The colonic macrophage phenotype was measured by mmunofluorescence and qPCR. The expression of Claudin-1, Occludin, ZO-1 and p-p65 was measured by western blot. The gene expression of peroxisome proliferator-activated receptor α (PPARα) and cytochrome P450 (CYP) 4X1 was determined using qPCR. Statistical analyses were performed using Student’s t-test for two-group comparisons, and one-way ANOVA followed by Student–Newman–Keul test for multiple-group comparisons. Results We observed intestinal barrier injury and gut microbiota dysbiosis characterized by Prevotellaceae and Rikenellaceae genus depletion and Escherichia-Shigella and Ruminococcaceae genus enrichment, accompanied by low butyrate production and M1-like polarization of colonic macrophages in BMS-1 (5 and 10 mg/kg)-induced cardiotoxicity. Fecal microbiota transplantation mirrored the effect of BMS-1 on cardiomyocyte apoptosis and cardiotoxicity, while macrophage depletion and neutralization of TNF-α and IL-1β greatly attenuated BMS-1-induced cardiotoxicity. Importantly, Prevotella loescheii recolonization and butyrate supplementation alleviated PD-1/PD-L1 inhibitor-related cardiotoxicity. Mechanistically, gut microbiota dysbiosis promoted M1-like polarization of colonic macrophages and the production of proinflammatory factors TNF-α and IL-1β through downregulation of PPARα-CYP4X1 axis. Conclusions Intestinal barrier dysfunction amplifies PD-1/PD-L1 inhibitor-related cardiotoxicity by upregulating proinflammatory factors TNF-α and IL-1β in colonic macrophages via downregulation of butyrate-PPARα-CYP4X1 axis. Thus, targeting gut microbiota to polarize colonic macrophages away from the M1-like phenotype could provide a potential therapeutic strategy for PD-1/PD-L1 inhibitor-related cardiotoxicity. Graphical abstract

scholarly journals Anethole Attenuates Enterotoxigenic Escherichia coli-Induced Intestinal Barrier Disruption and Intestinal Inflammation via Modification of TLR Signaling and Intestinal Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Qingyuan Yi ◽  
Jiaxin Liu ◽  
Yufeng Zhang ◽  
Hanzhen Qiao ◽  
Fang Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Performance ◽  
Mrna Expression ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Weaned Piglets ◽  
Tnf Α

This study aimed to investigate the effects of dietary anethole supplementation on the growth performance, intestinal barrier function, inflammatory response, and intestinal microbiota of piglets challenged with enterotoxigenic Escherichia coli K88. Thirty-six weaned piglets (24 ± 1 days old) were randomly allocated into four treatment groups: (1) sham challenge (CON); (2) Escherichia coli K88 challenge (ETEC); (3) Escherichia coli K88 challenge + antibiotics (ATB); and (4) Escherichia coli K88 challenge + anethole (AN). On day 12, the piglets in the ETEC, ATB, and AN group were challenged with 10 mL E. coli K88 (5 × 109 CFU/mL), whereas the piglets in the CON group were orally injected with 10 mL nutrient broth. On day 19, all the piglets were euthanized for sample collection. The results showed that the feed conversion ratio (FCR) was increased in the Escherichia coli K88-challenged piglets, which was reversed by the administration of antibiotics or anethole (P &lt; 0.05). The duodenum and jejunum of the piglets in ETEC group exhibited greater villous atrophy and intestinal morphology disruption than those of the piglets in CON, ATB, and AN groups (P &lt; 0.05). Administration of anethole protected intestinal barrier function and upregulated mucosal layer (mRNA expression of mucin-1 in the jejunum) and tight junction proteins (protein abundance of ZO-1 and Claudin-1 in the ileum) of the piglets challenged with Escherichia coli K88 (P &lt; 0.05). In addition, administration of antibiotics or anethole numerically reduced the plasma concentrations of IL-1β and TNF-α (P &lt; 0.1) and decreased the mRNA expression of TLR5, TLR9, MyD88, IL-1β, TNF-α, IL-6, and IL-10 in the jejunum of the piglets after challenge with Escherichia coli K88 (P &lt; 0.05). Dietary anethole supplementation enriched the abundance of beneficial flora in the intestines of the piglets. In summary, anethole can improve the growth performance of weaned piglets infected by ETEC through attenuating intestinal barrier disruption and intestinal inflammation.

scholarly journals Bacteriophage as an Alternative to Antibiotics Promotes Growth Performance by Regulating Intestinal Inflammation, Intestinal Barrier Function and Gut Microbiota in Weaned Piglets

2021 ◽  
Vol 8 ◽  
Author(s):  
Yongdi Zeng ◽  
Zirui Wang ◽  
Tiande Zou ◽  
Jun Chen ◽  
Guanhong Li ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Growth Performance ◽  
Barrier Function ◽  
Intestinal Inflammation ◽  
Control Diet ◽  
Intestinal Barrier ◽  
Basal Diet ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Weaned Piglets

This study aimed to investigate the effects of dietary bacteriophage supplementation on growth performance, intestinal morphology, barrier function, and intestinal microbiota of weaned piglets fed antibiotic-free diet. A total of 120 weaned piglets were allotted to four dietary treatments with five pens/treatment and six piglets/pen in a 21-d feeding trial. The control diet was supplemented with 25 mg/kg quinocetone and 11.25 mg/kg aureomycin in the basal diet, while the three treatment diets were supplemented with 200, 400, or 600 mg/kg bacteriophage in the basal diet, respectively. There was no difference for growth performance and all measured indices of serum and intestinal tissues between 200 mg/kg bacteriophage group and the control group with antibiotics (P &gt; 0.05). More importantly, compared with the control diet, dietary 400 mg/kg bacteriophage inclusion increased average daily gain and average daily feed intake, and decreased feed/gain ratio and diarrhea incidence of weaned piglets (P &lt; 0.05). Also, piglets fed 400 mg/kg bacteriophage had elevated villi height (VH) in jejunum and ileum, reduced crypt depth (CD) in jejunum and ileum, and elevated VH/CD ratio in duodenum, jejunum and ileum (P &lt; 0.05). Compared to the control group, piglets fed 400 mg/kg bacteriophage had lower interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and higher interleukin-10 (IL-10) concentration in serum, and higher secretory immunoglobulin A (sIgA), intestinal trefoil factor (ITF), and tumor growth factor-alpha (TGF-α) content in the ileal mucosa (P &lt; 0.05). Besides, dietary addition with 400 mg/kg bacteriophage decreased the D-lactate concentration and diamine oxidase (DAO) activity in serum, and increased the relative mRNA expression of ZO-1, Claudin-1, Occludin, TLR2, TLR4, and TLR9, as well as the relative protein expression of Occludin in the jejunum (P &lt; 0.05). However, the growth performance and all analyzed parameters in serum and intestinal tissues were not further improved when piglets fed 600 vs. 400 mg/kg bacteriophage (P &gt; 0.05). MiSeq sequencing analysis showed that bacteriophage regulated the microbial composition in caecum digesta, as indicated by higher observed_species, Chao1, and ACE richness indices, as well as changes in the relative abundance of Firmicutes, Bacteroidetes, and Tenericutes (P &lt; 0.05). Collectively, 400 mg/kg bacteriophage can be used as an antibiotics alternative for promoting the growth of weaned piglets. The underlying mechanism is associated with a positive effect of bacteriophage on intestinal inflammation, intestinal barrier function and gut microbiota in weaned piglets.

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