scholarly journals Salsola imbricata Forssk. ameliorates acetic acid-induced inflammatory bowel disease by modulating dysregulated antioxidant enzyme system and cytokine signaling pathways in mice

2021 ◽  
Vol 11 (12) ◽  
pp. 527
Author(s):  
Faraza Javed ◽  
Qaiser Jabeen
2018 ◽  
Vol 9 (8) ◽  
pp. 4143-4152 ◽  
Author(s):  
Shuai Chen ◽  
Meiwei Wang ◽  
Lanmei Yin ◽  
Wenkai Ren ◽  
Peng Bin ◽  
...  

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and is strongly associated with intestinal immunity and the microbiome.


2020 ◽  
Vol 19 (3) ◽  
pp. 629-636
Author(s):  
Kornsuda Thipart ◽  
Kutcharin Phunikhom ◽  
Acharaporn Na Lampang Noenplab ◽  
Jintana Sattayasai

Purpose: To investigate the effects of an aqueous extract of unpolished dark purple glutinous Thai rice, variety Luem pua (LP), in two rat models of inflammatory bowel disease (IBD). Methods: Polyphenolic compounds content were determined by HPLC methods and antioxidant activities by DPPH and FRAP assays of the LP extract. The effect of the LP extract at 5 g/kg/day were evaluated in two rat models of IBD that included acetic acid and indomethacin induced IBD. On each day of treatment, changes of body weight, stool consistency and stool blood were scored and expressed as disease activity index (DAI). At the end of the experiments, the animals were euthanized. Colon length and spleen weight were determined, and the degree of inflammation of the colon was scored. Results: Rats in both models of IBD (acetic acid- and indomethacin-induced IBD), exhibited significant increases in DAI, macroscopic inflammation scores and spleen weights, while the lengths of colon were decreased. Pretreatment with LP extract attenuated the disease severity in both models as seen by the reverse of all observed altered parameters. Conclusion: These data suggest that LP extract might be beneficial in preventing and/or treating IBD. Keywords: Inflammatory bowel disease (IBD), Dark purple glutinous rice Var. Luem Pua, Acetic acid, Indomethacin


2020 ◽  
Vol 5 (6) ◽  
pp. 17-26
Author(s):  
O. S. Zherebyatiev ◽  
◽  
O. V. Voitovich ◽  
T. Yu. Motilonok ◽  
A. A. Egorov ◽  
...  

Inflammatory bowel disease is an important illness of unclear pathogenesis associated with major defects in mucosal immunoregulation and develops in genetically susceptible individuals. These abnormalities often occur in association with microbial dysbiosis and result in unfettered inflammation of the intestine and extraintestinal tissues. Such events result in long-term morbidity and possibly even death, in otherwise healthy adults and children. Dampening inflammation and re-establishing immune tolerance in inflammatory bowel disease remain the major therapeutic goal. However, existing inflammatory bowel disease therapies albeit providing recent advances, still largely rely on broad-based immunosuppression. For example, only around half of the patients treated with anti-TNF agents show substantive clinical responses. These improvements are often self-limited, while unfortunately increasing the risk of opportunistic infections. The purpose of the study was to investigate the control of mucosal immune responses, which are based on fundamental signaling pathways. Long-term interests in the regulation of purinergic signaling are now being leveraged to develop innovative and hopefully non-toxic therapies for inflammatory bowel disease. This review and the accompanying articles in this special issue address new therapeutic concepts in inflammatory bowel disease, as based on recent, linked work in hypoxia and purinergic signaling, mucosal barrier functions and microRNA biology. In several recent, comprehensive reviews, have already addressed the biological functions of ectoenzymes, such as CD39, CD73, and CD38, in the regulation of purinergic signaling and control of extracellular adenosine levels. Others, have noted the importance of these mechanisms in immunomodulation, as in cancer and inflammation. The ectonucleotidases of the CD39 family, in particular, have major impacts on the dynamic equilibrium of proinflammatory extracellular ATP, ADP nucleotides vs. the immunosuppressive potential of adenosine nucleosides. CD39 plays a dominant role in purinergic regulation of vascular inflammation, thrombosis, and the immune response in such settings. The relevance and importance of these purinergic signaling pathways in selected neoplastic states (lymphoma and chronic leukemia) and inflammatory diseases (sepsis and autoimmunity) have been already alluded to in recent work. A brief synopsis of the major components of purinergic signaling; chiefly for those not familiar to this field, will focus on very recent work detailing the immunomodulation of CD39 on T cells and other immune cells by both genetic and environmental factors in the setting of inflammatory bowel disease and experimental colitis, inclusive of the new roles for natural metabolites such as bilirubin, and will also briefly cover the role of CD39 expression on exosomes and microparticles, in control of inflammation in the gut and touch on the relevance of the microbiome. Lastly, it will cover the emerging importance of other NTPDases of the CD39 family and speculate on their role in controlling gut inflammation. Conclusion. Review of the literature with own data is devoted to description of the recent advances in the study purinergic signaling pathways implicated in immune dysregulation, in the pathogenesis of inflammatory bowel disease. Our focus in this review is on novel aspects of the functions of CD39 and related nucleoside triphosphate diphosphohydrolases in inflammatory bowel disease


2019 ◽  
Vol 10 ◽  
Author(s):  
Tamara Pérez-Jeldres ◽  
Christopher J. Tyler ◽  
Joshua D. Boyer ◽  
Thangaraj Karuppuchamy ◽  
Andrés Yarur ◽  
...  

2016 ◽  
Vol 310 (3) ◽  
pp. G155-G162 ◽  
Author(s):  
Silvio Danese ◽  
Matthew Grisham ◽  
Jennifer Hodge ◽  
Jean-Baptiste Telliez

The inflammatory diseases ulcerative colitis and Crohn's disease constitute the two main forms of inflammatory bowel disease (IBD). They are characterized by chronic, relapsing inflammation of the gastrointestinal tract, significantly impacting on patient quality of life and often requiring prolonged treatment. Existing therapies for IBD are not effective for all patients, and an unmet need exists for additional therapies to induce and maintain remission. Here we describe the mechanism of action of the Janus kinase (JAK) inhibitor, tofacitinib, for the treatment of IBD and the effect of JAK inhibition on the chronic cycle of inflammation that is characteristic of the disease. The pathogenesis of IBD involves a dysfunctional response from the innate and adaptive immune system, resulting in overexpression of multiple inflammatory cytokines, many of which signal through JAKs. Thus JAK inhibition allows multiple cytokine signaling pathways to be targeted and is expected to modulate the innate and adaptive immune response in IBD, thereby interrupting the cycle of inflammation. Tofacitinib is an oral, small molecule JAK inhibitor that is being investigated as a targeted immunomodulator for IBD. Clinical development of tofacitinib and other JAK inhibitors is ongoing, with the aspiration of providing new treatment options for IBD that have the potential to deliver prolonged efficacy and clinically meaningful patient benefits.


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