039, P = 0.033, P = 0.001). The VMR on 40 and 60 mmHg CRD in 17β-estradiol Selleckchem isocitrate dehydrogenase inhibitor treated group was not significantly different from that in 17β-estradiol plus Ro25-6981 treated group. Whilst, significant differences of VMR were noted between 17β-estradiol treated group and 17β-estradiol plus AP5 treated group on 60, 80 mmHg CRD, respectively.17β-estradiol increased NR2B mRNA in anterior cingulate cortex (0.57 ± 0.41 vs 0.21 ± 0.13, P = 0.048), but not in dorsal root

ganglia (0.35 ± 0.45 vs 0.38 ± 0.31, P = 0.465). Stress-induced visceral hypersensitivity in the hormonally-restored visceral hyper-responsiveness of bilaterally ovariectomized rats was antagonized by AP5 or Ro25-6981. Conclusion: Estrogen may be mediated through NR2B activation to enhance visceral sensitivity in female stressed rats, that probably related with the inceased expression of NR2B mRNA in anterior cingulate cortex. Key Word(s): 1. IBS; 2. Estrogen; 3. Sress; 4. N-methyl-D-aspartate; CHIR-99021 cost Presenting Author: LU XIA Corresponding Author: LU XIA

Affiliations: Department of Gastroenterology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University Objective: Presence of intestinal microbes is considered a prerequisite for the development of ulcerative colitis (UC) including fungal community in the gut. However, there is little knowledge about the mechanisms. In the present study, we investigated the role of C-Type lectin receptor Dectin-1 in the regulation of anti-fungi selleck products immune responses in ulcerative colitis. Methods: The distribution of Dectin-1 in the gut were detected in biopsy tissues from UC patients and compared with normal controls by immunohistochemistry

and immunofluorescence staining. Dectin-1 expression levels were assessed from tissues in active UC patients, normal controls by RT-PCR and western bloting. We examined prevalence of fungi in human fecal and colonic mucosa, and identified the changes in fungal microbiome by PCR. Pripheral blood monouclear cells (PBMC) from healthy donors were co-cultured with zymosan, then we assessed the dectin-1 expression by flow cytometry and the production of inflammatory cytokines by ELISA. Results: Our results revealed an inverse relationship between dectin-1 expression and disease activity score in active UC patients. We demonstrated that the level of opportunistic pathogen fungus was higher than nonpathogenic fungus. Dectin-1 recognized theβ-glucan of fungal cell wall and bone marrow-derived monocyte responsed toβ-glucan producted inflammatory cytokines. In addition, Dectin-1 could crosstalk with TLRs and activate NF-κB by Myd88, SYK/CARD9 pathway. Finally, β-glucan particles zymosan could stimulate PBMC to express high level of Dectin-1 and produce high level of inflammatory cytokines. Conclusion: These findings suggest thatβ-glucan can interact with dectin-1 and activate NF-κB signaling pathway to regulate the inflammation process.