Daikenchuto and ITS Bioactive Compartment, Ginsenoside RB1 Enhanced Wound Healing of Intestinal Epithelial Cells

2017 ◽  
Vol 152 (5) ◽  
pp. S969
Author(s):  
Yuki Toyokawa ◽  
Tomohisa Takagi ◽  
Kazuhiko Uchiyama ◽  
Saori Kashiwagi ◽  
Yuji Naito ◽  
...  
2012 ◽  
Vol 142 (5) ◽  
pp. S-864
Author(s):  
Heike Dornhoff ◽  
Konstantin Fietkau ◽  
Sean Doyle ◽  
Markus F. Neurath ◽  
Jürgen Siebler

2009 ◽  
Vol 136 (5) ◽  
pp. A-700
Author(s):  
Geethanjali Pickert ◽  
Clemens Neufert ◽  
Moritz Leppkes ◽  
Alexei Nikolaev ◽  
Hans-Anton Lehr ◽  
...  

2009 ◽  
Vol 206 (7) ◽  
pp. 1465-1472 ◽  
Author(s):  
Geethanjali Pickert ◽  
Clemens Neufert ◽  
Moritz Leppkes ◽  
Yan Zheng ◽  
Nadine Wittkopf ◽  
...  

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22–dependent mucosal wound healing.


2007 ◽  
Vol 574 (2-3) ◽  
pp. 85-93 ◽  
Author(s):  
Bénédicte Buffin-Meyer ◽  
Pierre-Antoine Crassous ◽  
Christine Delage ◽  
Colette Denis ◽  
Stéphane Schaak ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Yongfei Bai ◽  
Yanmei Huang ◽  
Ying Li ◽  
Bingbing Zhang ◽  
Cuihong Xiao ◽  
...  

Lactobacillus casei (L. casei), a normal resident of the gastrointestinal tract of mammals, has been extensively studied over the past few decades for its probiotic properties in clinical and animal models. Some studies have shown that some bacterium of Lactobacillus stimulate the production of antimicrobial peptides in intestinal cells to clear enteric pathogens, however, which antimicrobial peptides are produced by L. casei stimulation and its function are still not completely understood. In this study, we investigated the changes of antimicrobial peptides’ expression after intragastric administration of L. casei to mice. The bioinformatics analysis revealed there were nine genes strongly associated with up-regulated DEGs. But, of these, only the antimicrobial peptide mReg3a gene was continuously up-regulated, which was also confirmed by qRT-PCR. We found out the mReg3a expressed in engineering E.coli promoted cell proliferation and wound healing proved by CCK-8 assay and wound healing assay. Moreover, the tight junction proteins ZO-1 and E-cadherin in mReg3a treatment group were significantly higher than that in the control group under the final concentration of 0.2 mg/ml both in Porcine intestinal epithelial cells (IPEC-J2) and Mouse intestinal epithelial cells (IEC-6) (p < 0.05). Surprisingly, the recombinant mReg3a not only inhibited Enterotoxigenic Escherichia coli (ETEC), but also reduced the copy number of the piglet diarrheal viruses, porcine epidemic diarrhea virus (PEDV), porcine transmissible gastroenteritis virus (TGEV), and porcine rotavirus (PoRV), indicating the antimicrobial peptides mReg3a may be feed additives to resist the potential of the intestinal bacterial and viral diarrhea disease.


Sign in / Sign up

Export Citation Format

Share Document