Abstract

To determine the effects of heat-killed VSL#3 (B. breve, B. longum and B. infantis; L. plantarum, L. bulgaricus, L. casei and L. acidophilus; S. salivarius subsp. thermophilus) therapy in the dextran sulfate sodium (DSS)-induced acute experimental colitis in rats. Acute experimental colitis was induced in rats by 5% DSS and freely drink for seven days. Beginning on Day 8, rats underwent gavage once daily for seven days with heat-killed probiotic VSL#3 (0.6 g/kg/day), colonic damage was evaluated histologically and biochemically seven days after gavage. Expression of inflammatory related mediators (STAT3, P-STAT3) and cytokines (IL-6, IL-23, TGFβ) in colonic tissue were detected. The results revealed that heat-killed and live VSL#3 have identical anti-inflammatory properties by the assessed DAI (disease activity index), colon length, histological tissue and MPO activity. Heat-killed and live VSL#3 results in reduced IL-6, IL-23, TGFβ, STAT3 and P-STAT3 expression in colonic tissue. Heat-killed and live VSL#3 have showed the similar anti-inflammatory activity by inhibiting IL-6/STAT3 pathway in the DSS-induced acute experimental colitis in rats.

Highlights

  • Inflammatory bowel disease (IBD) is a set of chronic recurrent diseases, including ulcerative colitis (UC) and Crohn’s disease (CD)

  • It has been shown that genetic factors, environmental factors, intestinal flora disturbance and immune dysregulation may involve in pathogenesis of IBD

  • We examined the effect of probiotic VSL#3 and heat-killed VSL#3 on the protein expression of IL-6, IL-23, TGF-β, STAT3 and P-STAT3 proteins in the colons of rats of each group by Western-blot

Read more

Summary

Introduction

Inflammatory bowel disease (IBD) is a set of chronic recurrent diseases, including ulcerative colitis (UC) and Crohn’s disease (CD). The exact pathogenic mechanism of IBD remains unclear but several possible mechanisms have been clarified. It has been shown that genetic factors, environmental factors, intestinal flora disturbance and immune dysregulation may involve in pathogenesis of IBD. More than four million people worldwide suffer from IBD. Medical therapies for IBD include 5-aminosalicylic acid drugs, methotrexate, immunomodulators and biological therapies (mainly anti-tumor necrosis factor). The high cost, multiple adverse effects and limited effect prompt research and development of new treatment options

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call