NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

RSC Advances ◽  
2016 ◽  
Vol 6 (69) ◽  
pp. 64208-64214 ◽  
Author(s):  
Shenglan Yang ◽  
Danfang Deng ◽  
Yingying Luo ◽  
Yanran Wu ◽  
Rui Zhu ◽  
...  

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells.

2001 ◽  
Vol 120 (5) ◽  
pp. A714-A714
Author(s):  
H AKIHO ◽  
R DEGIORGIO ◽  
G BARBARA ◽  
P BLENNERHASSETT ◽  
Y DENG ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A714
Author(s):  
Hirotada Akiho ◽  
Roberto Degiorgio ◽  
Giovanni Barbara ◽  
Patricia A. Blennerhassett ◽  
Yikang Deng ◽  
...  

2007 ◽  
Vol 35 (5) ◽  
pp. 583-589 ◽  
Author(s):  
M Guslandi

Irritable bowel syndrome (IBS) is characterized by abdominal pain and alterations in bowel habits. Several pathogenetic factors, such as altered intestinal motility, visceral hypersensitivity, serotonin system abnormalities and psychic disturbances have been identified. Recently, a pathogenetic role of intestinal microflora has been shown in IBS: viral or bacterial infection can trigger post-infectious IBS; some patients have small intestinal bacterial overgrowth; the composition of patients' enteric flora is altered; and minimal inflammatory changes, consistent with the pro-inflammatory role of bacteria, have been demonstrated. Probiotics may, therefore, offer a rational therapeutic approach to IBS. The data available on the use of probiotics in IBS are still limited and results of controlled clinical trials are contradictory because they have been performed using different species, dosages, treatment durations and end-points for results evaluation. A critical evaluation of the therapeutic role of the various probiotics in IBS is presented in this article.


Medicina ◽  
2020 ◽  
Vol 56 (4) ◽  
pp. 175 ◽  
Author(s):  
Ioana-Miruna Balmus ◽  
Alin Ciobica ◽  
Roxana Cojocariu ◽  
Alina-Costina Luca ◽  
Lucian Gorgan

Background: Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, exhibiting complex and controversial pathological features. Both oxidative stress and inflammation-related reactive oxygen species production may be involved in IBS pathological development. Thus, we focused on several aspects regarding the causes of oxidative stress occurrence in IBS. Additionally, in the molecular context of oxidative changes, we tried to discuss these possible neurological implications in IBS. Methods: The literature search included the main available databases (e.g., ScienceDirect, Pubmed/Medline, Embase, and Google Scholar). Articles in the English language were taken into consideration. Our screening was conducted based on several words such as “irritable bowel syndrome”, “gut brain axis”, “oxidative stress”, “neuroendocrine”, and combinations. Results: While no consistent evidence suggests clear pathway mechanisms, it seems that the inflammatory response may also be relevant in IBS. The mild implication of oxidative stress in IBS has been described through clinical studies and some animal models, revealing changes in the main markers such as antioxidant status and peroxidation markers. Moreover, it seems that the neurological structures involved in the brain-gut axis may be affected in IBS rather than the local gut tissue and functionality. Due to a gut-brain axis bidirectional communication error, a correlation between neurological impairment, emotional over-responsiveness, mild inflammatory patterns, and oxidative stress can be suggested. Conclusions: Therefore, there is a possible correlation between neurological impairment, emotional over-responsiveness, mild inflammatory patterns, and oxidative stress that are not followed by tissue destruction in IBS patients. Moreover, it is not yet clear whether oxidative stress, inflammation, or neurological impairments are key determinants or in which way these three interact in IBS pathology. However, the conditions in which oxidative imbalances occur may be an interesting research lead in order to find possible explanations for IBS development.


2020 ◽  
Vol 21 (15) ◽  
pp. 5575
Author(s):  
Adam J. Bittel ◽  
Sen Chandra Sreetama ◽  
Daniel C. Bittel ◽  
Adam Horn ◽  
James S. Novak ◽  
...  

Deficits in plasma membrane repair have been identified in dysferlinopathy and Duchenne Muscular Dystrophy, and contribute to progressive myopathy. Although Facioscapulohumeral Muscular Dystrophy (FSHD) shares clinicopathological features with these muscular dystrophies, it is unknown if FSHD is characterized by plasma membrane repair deficits. Therefore, we exposed immortalized human FSHD myoblasts, immortalized myoblasts from unaffected siblings, and myofibers from a murine model of FSHD (FLExDUX4) to focal, pulsed laser ablation of the sarcolemma. Repair kinetics and success were determined from the accumulation of intracellular FM1-43 dye post-injury. We subsequently treated FSHD myoblasts with a DUX4-targeting antisense oligonucleotide (AON) to reduce DUX4 expression, and with the antioxidant Trolox to determine the role of DUX4 expression and oxidative stress in membrane repair. Compared to unaffected myoblasts, FSHD myoblasts demonstrate poor repair and a greater percentage of cells that failed to repair, which was mitigated by AON and Trolox treatments. Similar repair deficits were identified in FLExDUX4 myofibers. This is the first study to identify plasma membrane repair deficits in myoblasts from individuals with FSHD, and in myofibers from a murine model of FSHD. Our results suggest that DUX4 expression and oxidative stress may be important targets for future membrane-repair therapies.


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