scholarly journals ACTION OF DONORS OF HYDROGEN SULFIDE ON THE PARAMETERS OF OXIDATIVE STRESS IN SMALL INTESTINAL MUCOSA OF RATS UNDER CONDITIONS OF THE ENALAPRIL ACTION

2018 ◽  
Vol 1 (2) ◽  
pp. 172
Author(s):  
Yu. O. Sklyarova ◽  
I. S. Fomenko
2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zhongshen Kuang ◽  
Tingting Jin ◽  
ChangYi Wu ◽  
Yanan Zong ◽  
Panpan Yin ◽  
...  

This study is aimed at exploring the effects of lentinan on small intestinal mucosa as well as lung and liver injury in mice with gut-origin sepsis. Cecal ligation and perforation (CLP) were used to construct a mouse model of gut-origin sepsis. The mice were randomly divided into six groups: sham operation group (sham), gut-origin sepsis model group (CLP), ulinastatin-positive drug control group (UTI), lentinan low concentration group (LTN-L, 5 mg/kg), lentinan medium concentration group (LTN-M, 10 mg/kg), and lentinan high concentration group (LTN-H, 20 mg/kg). H&E staining was used to detect the pathological damage of the small intestine, liver, and lung. The serum of mice in each group was collected to detect the expression changes of inflammatory cytokines, oxidative stress biomarkers, and liver function indexes. In vitro assessment of bacterial translocation was achieved through inoculated culture media. Western blot and RT-qPCR were used to detect the expression of molecules related to the NF-κB signaling pathway in the small intestine tissues of mice. The results showed that compared with the CLP group, the injury degree of the small intestine, liver, and lung in mice with gut-origin sepsis was improved with the increase of lentinan concentration. In addition, TNF-α, IL-1β, IL-6, and HMGB1 were decreased with the increase of lentinan concentration, but the expression of IL-10 was increased. Lentinan could also reduce the expression of oxidative stress injury indexes and liver function indexes and inhibit bacterial translocation to liver and lung tissues. Further mechanism investigation revealed that lentinan downregulated the expression of the NF-κB signaling pathway molecules (NF-κB, TLR4, and Bax) and upregulated the expression of occludin and Bcl-2. In conclusion, lentinan inhibits the activity of the NF-κB signaling pathway, thus attenuating injuries of small intestinal mucosa and liver and lung in mice with gut-origin sepsis and reducing the inflammatory response in the process of sepsis.


Author(s):  
Yu. O. Sklyarova ◽  
I. S. Fomenko

Introduction. Medication-induced enteropathy plays an important part among factors leading to the development of small intestinal injury. There are some evidences indicating a potential preventive action of hydrogen sulfide (H2S) donors against drug-induced enteropathies based on that fact that the use of the most of enterotoxic medications including anti-tumor drugs leads to the suppression of this gaseous mediator production. The aim of the study – to compare the action of H2S donors in small intestine of rats on parameters of NO-synthase system and oxidative stress under condition of methotrexate-induced enteropathy. Research Methods. The experimental procedures were carried out on rats which on the background of methotrexate-induced enteropathy received H2S donors NaHS (1 and 10 mg/kg) and L-cysteine. Following biochemical parameters were measured in small intestinal mucosa: activity of NO-synthases, myeloperoxidase, superoxide dismutase and catalase; concentrations of NOx (nitrite/nitrate) and malonic dialdehyde. H2S concentration was determined in blood serum. Results and Discussion. Administration of methotrexate didn’t cause any visible changes of small intestine surface, however led to serious biochemical changes. NO concentration increased as a result of iNOS activation (more than fivefold (p≤0.01). Simultaneously concentration of H2S decreased in blood serum. Administration of H2.S donors practically returned these parameters to their normal value. Methotrexate-induced enteropathy caused the increase of myeloperoxidase activity by 66 %, p≤0.01, indicating of inflammatory process formation and activation of lipid peroxidation. Administration of NaHS didn’t cause any serious changes in myeloperoxidase activity, however increased SOD activity and practically retuned it to its norm. Conclusions. Nirtoso-oxidative stress plays the key role in enteropathy formation resulted in methotrexate administration. H2S donors modulate parameters of NO-synthase system and activity of SOD.


2009 ◽  
Vol 102 (9) ◽  
pp. 1285-1296 ◽  
Author(s):  
Maud Le Gall ◽  
Mélanie Gallois ◽  
Bernard Sève ◽  
Isabelle Louveau ◽  
Jens J. Holst ◽  
...  

Sodium butyrate (SB) provided orally favours body growth and maturation of the gastrointestinal tract (GIT) in milk-fed pigs. In weaned pigs, conflicting results have been obtained. Therefore, we hypothesised that the effects of SB (3 g/kg DM intake) depend on the period (before v. after weaning) of its oral administration. From the age of 5 d, thirty-two pigs, blocked in quadruplicates within litters, were assigned to one of four treatments: no SB (control), SB before (for 24 d), or after (for 11–12 d) weaning and SB before and after weaning (for 35–36 d). Growth performance, feed intake and various end-point indices of GIT anatomy and physiology were investigated at slaughter. The pigs supplemented with SB before weaning grew faster after weaning than the controls (P < 0·05). The feed intake was higher in pigs supplemented with SB before or after weaning (P < 0·05). SB provided before weaning improved post-weaning faecal digestibility (P < 0·05) while SB after weaning decreased ileal and faecal digestibilities (P < 0·05). Gastric digesta retention was higher when SB was provided before weaning (P < 0·05). Post-weaning administration of SB decreased the activity of three pancreatic enzymes and five intestinal enzymes (P < 0·05). IL-18 gene expression tended to be lower in the mid-jejunum in SB-supplemented pigs. The small-intestinal mucosa was thinner and jejunal villous height lower in all SB groups (P < 0·05). In conclusion, the pre-weaning SB supplementation was the most efficient to stimulate body growth and feed intake after weaning, by reducing gastric emptying and intestinal mucosa weight and by increasing feed digestibility.


1984 ◽  
Vol 259 (4) ◽  
pp. 2452-2456 ◽  
Author(s):  
M C Blaufuss ◽  
J I Gordon ◽  
G Schonfeld ◽  
A W Strauss ◽  
D H Alpers

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