scholarly journals The Effect of Dietary Quercetin on the Glutathione Redox System and Small Intestinal Functionality of Weaned Piglets

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 312 ◽  
Author(s):  
Jeroen Degroote ◽  
Hans Vergauwen ◽  
Noémie Van Noten ◽  
Wei Wang ◽  
Stefaan De Smet ◽  
...  

Quercetin has been shown to alleviate mucosal damage and modulate the glutathione (GSH) redox system in the colon of rodents. In the current study, we assessed whether quercetin was able to mitigate small intestinal dysfunction in weaned pigs. Here, 224 weaned piglets were fed a diet containing quercetin at either 0, 100, 300, or 900 mg/kg diet until d14 post-weaning, followed by a common basal diet until d42. Eight animals per treatment were sampled at d5 and d14 post-weaning. In these animals, the small intestinal histomorphology, barrier function, and protein abundance of occludin, caspase-3, and proliferating cell nuclear antigen were assessed. None of these parameters were affected, and neither did quercetin improve performance up to d42 post-weaning. The GSH redox system was evaluated in blood, small intestinal mucosa, and liver. Quercetin did not affect the glutathione peroxidase, glutathione reductase, and glutamate–cysteine ligase activity in these tissues. In contrast, the hepatic glutathione transferase (GST) activity was significantly increased by quercetin supplementation at d5 post-weaning of 100, 300, and 900 mg/kg. Importantly, d5 was characterized by a more oxidized GSH redox status. To conclude, dietary quercetin had little effect on the small intestine, but did upregulate hepatic GST in the occurrence of redox disturbance.

Author(s):  
Kaiwen Bai ◽  
Luyi Jiang ◽  
Qiming Li ◽  
Jingfei Zhang ◽  
Lili Zhang ◽  
...  

Abstract Few studies have focused on the role of dimethylglycine sodium salt (DMG-Na) in protecting the redox status of skeletal muscle, although it is reported to be beneficial in animal husbandry. This study investigated the beneficial effects of DMG-Na on the growth performance, longissimus dorsi muscle (LM) redox status, and mitochondrial function in weaning piglets that were intrauterine growth restricted (IUGR). Ten normal birth weight (NBW) newborn piglets (1.53 ± 0.04 kg) and 20 IUGR newborn piglets (0.76 ± 0.06 kg) from ten sows were obtained. All piglets were weaned at 21 days of age and allocated to three groups with ten replicates per group: NBW-weaned piglets fed a common basal diet (N); IUGR weaned piglets fed a common basal diet (I); IUGR weaned piglets fed a common basal diet supplemented with 0.1% DMG-Na (ID). They were slaughtered at 49 days of age to collect the serum and LM samples. Compared with the N group, the growth performance, LM structure, serum, and, within the LM, mitochondrial redox status, mitochondrial respiratory chain complex activity, energy metabolites, redox status-related, cell adhesion-related, and mitochondrial function-related gene expression, and protein expression deteriorated in group I (P < 0.05). The ID group showed improved growth performance, LM structure, serum, and, within the LM, mitochondrial redox status, mitochondrial respiratory chain complex activity, energy metabolites, redox status-related, cell adhesion-related, and mitochondrial function-related gene expression, and protein expression compared with those in the I group (P < 0.05). The above results indicated that the DMG-Na treatment could improve the LM redox status and mitochondrial function in IUGR weaned piglets via the Nuclear factor erythroid 2-related factor 2 (Nrf2)/ Sirtuin 1 (SIRT1)/ Peroxisome proliferator-activated receptorγcoactivator-1α (PGC1α) network, thus improving their growth performance.


2020 ◽  
Vol 60 (16) ◽  
pp. 1894
Author(s):  
Huishi Yan ◽  
Wenwei Gao ◽  
Qinghong Li ◽  
Hongquan Li ◽  
Ruirong Hao

Context Grapeseed procyanidins (GSP) are widely recognised to have potential biological properties, and dietary supplementation with GSP could reduce diarrhoea incidence in weaned piglets. Aims This trial was conducted to investigate the effect of GSP on small intestinal mucosa morphology and small intestinal development in weaned piglets. Methods Seventy-two weaned piglets were randomly allocated into four dietary groups with three replicate pens per group and six piglets per pen. Each group received one of the following diets: a basal maize–soybean meal diet; or basal diet supplemented with 50, 100 or 150 mg GSP/kg. Small intestinal mucosa morphology and the expression of genes involved in improving small intestinal development were determined. Key results Morphological observations obtained by optical microscopy showed that the villus height of the duodenum and ileum increased in all groups receiving GSP, significantly (P < 0.05) so in the group receiving 100 mg GSP/kg compared with the control group. Crypt depth of the duodenum and ileum in the groups receiving 100 and 150 mg GSP/kg decreased compared with the control group. Similarly, the crypt depth of the jejunum in the group receiving 100 mg GSP/kg was significantly (P < 0.05) lowered. Moreover, the villus height/crypt depth ratio of each small intestinal segment in the group receiving 100 mg GSP/kg increased significantly (P < 0.01). Morphological observations obtained by scanning electron microscopy indicated that dietary supplementation with GSP was favourable for growth of small intestinal villi. Specifically, the villi of the small intestine in the group receiving 100 mg GSP/kg were most closely aligned, most uniform in size and clearest in structure. Furthermore, dietary supplementation with GSP increased the expression of genes encoding epidermal growth factor receptor, insulin-like growth factor 1 (IGF-1) and IGF-1 receptor in the duodenum, the group receiving 100 mg GSP/kg showing a significant (P < 0.05) increase. Conclusions Dietary supplementation with GSP could improve small intestinal mucosa morphology and promote small intestinal development. Dietary supplementation of 100 mg GSP/kg could be recommended for weaned piglets. Implications Dietary supplementation with GSP generated a beneficial role in small intestinal health in weaned piglets.


Author(s):  
Làszló G. Kömüves

In the small intestinal mucosa of healthy adult mammals proliferating cell are confined to the crypts of Lieberkiihn. Earlier radioautographic studies identified proliferative cells in the small intestine of several non-mammalian vertebrates. However, it is still not clear whether cell renewal is confined to proliferative compartment within the small intestinal mucosa in non-mammalian vertebrates. In the present study proliferative cells were identified using an immunological marker of cell proliferation, the proliferating cell nuclear antigen (PCNA) in the small intestine of several non-mammalian vertebrate species, including birds (zebrafinch, Poephila guttata), reptiles (green anole, Anolis carolinensis), amphibia (axolotl, Ambystoma mexicanum), and fishes (goldfish, Carassius auratus).Segments of the small intestine were fixed in 4% formaldehyde in 0.86 M phosphate buffer, pH=7.2 and embedded in paraffin. Deparaffinized and rehydrated sections were microwaved in citrate buffer. The immunohistochemical detection method used in this study based on the capillary action principle, as developed by Brigati.


2009 ◽  
Vol 89 (2) ◽  
pp. 253-262 ◽  
Author(s):  
Y J Wang ◽  
M. Ko ◽  
S. Holligan ◽  
B W McBride ◽  
M Z Fan ◽  
...  

Twenty-four steers [467 ± 7.2 kg initial body weight (BW)] predominately of Angus breeding were used to determine the effect of dry matter intake (1.25, 1.50, 1.75, and 2.00% of BW) on visceral mass, cellularity, and the protein expression of ATP synthase, Na+/K+-ATPase, proliferating cell nuclear antigen (PCNA) and ubiquitin. There were linear increases (P ≤ 0.05) in weights of total viscera, total digestive tract, liver, kidney, heart, lung, spleen, rumen, and abomasum with increasing dry matter intake (DMI). Protein concentration decreased linearly (P < 0.05) in small intestinal mucosa as DMI increased. PCNA expression increased linearly (P < 0.01) in liver as DMI increased. PCNA expression was affected quadratically (P < 0.05) in pancreas and small intestinal mucosa with an increase when DMI increased from 1.25 to 1.75% of BW, and a decrease when DMI increased from 1.75 to 2% of BW. ATP synthase, Na+/K+-ATPase, and ubiquitin expression in pancreas and ubiquitin expression in small intestinal mucosa increased linearly (P < 0.05) as DMI increased. These results indicate that increasing DMI increases the mass of visceral organs and carcass and influences expression of proteins influencing energy utilization and efficiency in pancreas, small intestine, liver, and sternomandibularis muscle.Key words: Dry matter intake, visceral organ mass, cellular energy metabolism, steer


Blood ◽  
1994 ◽  
Vol 83 (1) ◽  
pp. 33-37 ◽  
Author(s):  
XX Du ◽  
CM Doerschuk ◽  
A Orazi ◽  
DA Williams

The proliferation of epithelial cells lining the small intestinal mucosa may be regulated by microenvironmental signals leading to differentiation of precursor cells in the small intestinal crypts. Proliferation of hematopoietic cells within the hematopoietic microenvironment is known to be regulated by a growing number of glycoprotein growth factors in a hierarchial fashion. We studied the effects of administration of the microenvironment-derived hematopoietic growth factor interleukin-11 (IL-11) on mice given combination radiation/chemotherapy. Treatment of such mice with IL-11 led to significantly increased survival and evidence of rapid recovery of the small intestinal mucosa, which is severely damaged by these cytoxic agents. This recovery was associated with an increase in the mitotic index of crypt cells and an increased frequency of staining of these cells with a monoclonal antibody to proliferating cell nuclear antigen, a member of the cyclin family of nuclear antigens.


2004 ◽  
Vol 107 (3) ◽  
pp. 281-289 ◽  
Author(s):  
Jayasree BASIVIREDDY ◽  
Molly JACOB ◽  
Kunissery A. BALASUBRAMANIAN

The use of NSAIDs (non-steroidal anti-inflammatory drugs), although of great therapeutic value clinically, is limited by their tendency to cause mucosal damage in the gastrointestinal tract. In the small intestine, the effects these drugs have been shown to produce include inhibition of cyclo-oxygenase, mitochondrial dysfunction and free radical-induced oxidative changes, all of which contribute to the mucosal damage seen. Glutamine is a fuel preferentially used by enterocytes and is known to contribute to maintaining the integrity of these cells. In the present study, we investigated the effect of glutamine on indomethacin-induced changes in the small intestinal mucosa. Rats were given 2% glutamine or glutamic acid or isonitrogenous amino acids, glycine or alanine, in the diet for 7 days. Indomethacin was then administered orally at a dose of 40 mg/kg of body weight. After 1 h, the small intestine was removed and used for the measurement of parameters of oxidative stress and mitochondrial and BBM (brush border membrane) function. Evidence of oxidative stress was found in the mucosa of the small intestine of drug-treated rats, as indicated by significantly increased activity of xanthine oxidase (P<0.001) and myeloperoxidase (P<0.001), with corresponding decreases in the levels of several free radical scavenging enzymes and α-tocopherol (P<0.001 in all cases). Levels of products of peroxidation were also significantly elevated (P<0.001 for all the parameters measured). In addition, oxidative stress was evident in isolated intestinal mitochondria and BBMs (P<0.001 for all the parameters measured), with associated alterations in function of these organelles (P<0.001 for all the parameters measured). Supplementation of the diet with glutamine or glutamic acid prior to treatment with indomethacin produced significant amelioration in all the effects produced by the drug in the small intestine (P<0.001 for all the parameters measured). Glycine and alanine were found to be much less effective in these respects.


Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 575 ◽  
Author(s):  
Jingle Jiang ◽  
Lina Qi ◽  
Zengpeng Lv ◽  
Song Jin ◽  
Xihui Wei ◽  
...  

The study was conducted to investigate the effects of dietary stevioside (STE) supplementation on the lipopolysaccharide (LPS)-induced intestinal mucosal damage of broiler chickens. A total of 192 one-day-old male Ross 308 broiler chicks were randomly divided into four treatments: (1) basal diet (CON); (2) basal diet supplemented with 250 mg/kg stevioside (STE); (3) basal diet + LPS-challenge (LPS); (4) basal diet supplemented with 250 mg/kg stevioside + LPS-challenge (LPS + STE). LPS-challenged groups received an intraperitoneal injection of LPS at 17, 19 and 21 d, whereas the CON and STE groups received a saline injection. The results showed that dietary STE supplementation normalized LPS-induced changes in protein expression of p-NF-κB and p-IκBα, mRNA expression of inflammatory genes (TLR4, NF-κB, and IFN-γ), tight junction-related genes (CLDN2, OCLN, and ZO-1), and antioxidant genes (Nrf2 and HO-1). LPS-induced decreases in serum diamine oxidase (DAO) level, villus height-to-crypt depth ratio, apoptotic index, and protein expression of proliferating cell nuclear antigen (PCNA) were reversed with dietary STE supplementation. Additionally, STE supplementation ameliorated the redox damage by reducing malondialdehyde (MDA) content and increasing total antioxidant capacity (T-AOC) and antioxidant enzyme activity. In conclusion, dietary stevioside supplementation could alleviate LPS-induced intestinal mucosal damage through anti-inflammatory and antioxidant effects in broiler chickens.


Blood ◽  
1994 ◽  
Vol 83 (1) ◽  
pp. 33-37 ◽  
Author(s):  
XX Du ◽  
CM Doerschuk ◽  
A Orazi ◽  
DA Williams

Abstract The proliferation of epithelial cells lining the small intestinal mucosa may be regulated by microenvironmental signals leading to differentiation of precursor cells in the small intestinal crypts. Proliferation of hematopoietic cells within the hematopoietic microenvironment is known to be regulated by a growing number of glycoprotein growth factors in a hierarchial fashion. We studied the effects of administration of the microenvironment-derived hematopoietic growth factor interleukin-11 (IL-11) on mice given combination radiation/chemotherapy. Treatment of such mice with IL-11 led to significantly increased survival and evidence of rapid recovery of the small intestinal mucosa, which is severely damaged by these cytoxic agents. This recovery was associated with an increase in the mitotic index of crypt cells and an increased frequency of staining of these cells with a monoclonal antibody to proliferating cell nuclear antigen, a member of the cyclin family of nuclear antigens.


Antioxidants ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 24 ◽  
Author(s):  
Jeroen Degroote ◽  
Noémie Van Noten ◽  
Wei Wang ◽  
Stefaan De Smet ◽  
Joris Michiels

This study investigated the effect of N-acetyl-cysteine (NAC) supplementation through drinking water on animal performance and the glutathione (GSH) redox system in weaned piglets, particularly in relation to the immediate post-weaning feed intake. To this end, 168 piglets were weaned and either fed ad libitum or fasted the first two days, and either or not administered 200 mg/L NAC via the drinking water until d14 post-weaning. Next to animal performance until day 42 (d42), the GSH redox system was measured in erythrocytes, small intestinal mucosa, liver, lung, and kidney tissue at d0, d2, and d14 post-weaning. Animal performance and GSH levels were not affected by NAC, nor by fasting. Irrespective of treatment, a significant drop in GSH at d2 post-weaning was found as compared to d0, in particular in liver (−69%), distal jejunal mucosa (−72%), and lung tissue (−80%). Post-weaning changes of the GSH redox status were strongly tissue-dependent. To conclude, this research indicates that GSH redox homeostasis was largely affected in multiple organs during the weaning transition. NAC supplementation did not increase GSH levels in any tissue, not even in fasted animals, questioning the fact if cysteine is the first or only limiting factor determining the rate of GSH synthesis in the early post-weaning phase.


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