A smart cauliflower-like carrier for astaxanthin delivery to relieve colon inflammation

Author(s):  
Xuedi Zhang ◽  
Xue Zhao ◽  
Shanshan Tie ◽  
Jiaxuan Li ◽  
Wentao Su ◽  
...  
Keyword(s):  
2021 ◽  
Vol 160 (6) ◽  
pp. S-325-S-326
Author(s):  
Ahmed Elfiky ◽  
Ishtu Hageman ◽  
Patricia Van Hamersveld ◽  
Olaf Welting ◽  
Jan Verhoeff ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masahiro Kitabatake ◽  
Yoko Matsumura ◽  
Noriko Ouji-Sageshima ◽  
Tatsuki Nishioka ◽  
Atsushi Hara ◽  
...  

AbstractUlcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) induced by dysregulation of the immune response in the intestinal mucosa. Although the underlying mechanisms of UC development are not fully understood, disruption of gut microbiota, “dysbiosis”, is thought to lead to the development of IBD. Persimmon (Ebenaceae Diospyros kaki Thunb.)-derived tannin, which is a condensed polymeric tannin consisting of catechin groups, has antioxidant, anti-inflammatory, and antimicrobial activities. In this study, we assessed the effect of persimmon-derived tannin on a murine model of UC established by dextran sulfate sodium-induced colitis in female mice. Dietary supplementation of tannin significantly decreased disease activity and colon inflammation. A hydrolysate of tannin directly suppressed expression of inflammatory genes in macrophages in vitro. In faecal microbiota, the relative abundance of Bacteroides was increased significantly by tannin supplementation. Alpha-diversity indices in colitis-induced mice were significantly higher in the tannin diet group compared with the control diet group. Additionally, expansion of Enterobacteriaceae and Enterococcus, which is associated with disease progression of IBD, was remarkably suppressed in the tannin diet group. These results suggest that persimmon-derived tannin ameliorates colon inflammation in UC through alteration of the microbiota composition and immune response, which may be a promising candidate for IBD therapy.


2009 ◽  
Vol 297 (6) ◽  
pp. G1250-G1258 ◽  
Author(s):  
Pablo Rodolfo Brumovsky ◽  
Bin Feng ◽  
Linjing Xu ◽  
Carly Jane McCarthy ◽  
G. F. Gebhart

Studies in humans and rodents suggest that colon inflammation promotes urinary bladder hypersensitivity and, conversely, that cystitis contributes to colon hypersensitivity, events referred to as cross-organ sensitization. To investigate a potential peripheral mechanism, we examined whether cystitis alters the sensitivity of pelvic nerve colorectal afferents. Male C57BL/6 mice were treated with cyclophosphamide (CYP) or saline, and the mechanosensitive properties of single afferent fibers innervating the colorectum were studied with an in vitro preparation. In addition, mechanosensitive receptive endings were exposed to an inflammatory soup (IS) to study sensitization. Urinary bladder mechanosensitive afferents were also tested. We found that baseline responses of stretch-sensitive colorectal afferents did not differ between treatment groups. Whereas IS excited a proportion of colorectal afferents CYP treatment did not alter the magnitude of this response. However, the number of stretch-sensitive fibers excited by IS was increased relative to saline-treated mice. Responses to IS were not altered by CYP treatment, but the proportion of IS-responsive fibers was increased relative to saline-treated mice. In bladder, IS application increased responses of muscular afferents to stretch, although no differences were detected between saline- and CYP-treated mice. In contrast, their chemosensitivity to IS was decreased in the CYP-treated group. Histological examination revealed no changes in colorectum and modest edema and infiltration in the urinary bladder of CYP-treated mice. In conclusion, CYP treatment increased mechanical sensitivity of colorectal muscular afferents and increased the proportion of chemosensitive colorectal afferents. These data support a peripheral contribution to cross-organ sensitization of pelvic organs.


2000 ◽  
Vol 118 (4) ◽  
pp. A864 ◽  
Author(s):  
Laurent Dubuquoy ◽  
Pierre Desreumaux ◽  
Michel Peuchmaur ◽  
Benoit Derijard ◽  
Sophie Nutten ◽  
...  

2018 ◽  
Vol 115 (52) ◽  
pp. E12313-E12322 ◽  
Author(s):  
Tingting Zheng ◽  
Baohua Zhang ◽  
Ce Chen ◽  
Jingyu Ma ◽  
Deyun Meng ◽  
...  

Dendritic cells (DCs) play pivotal roles in maintaining intestinal homeostasis, but how the DCs regulate diverse immune networks on homeostasis breakdown remains largely unknown. Here, we report that, in response to epithelial barrier disruption, colonic DCs regulate the differentiation of type 1 regulatory T (Tr1) cells through p38α-dependent IL-27 production to initiate an effective immune response. Deletion of p38α in DCs, but not in T cells, led to increased Tr1 and protected mice from dextran sodium sulfate-induced acute colitis and chronic colitis-associated colorectal cancer. We show that higher levels of IL-27 in p38α-deficient colonic cDC1s, but not cDC2s, were responsible for the increase of Tr1 cells. Moreover, p38α-dependent IL-27 enhanced IL-22 secretion from intestinal group 3 innate lymphoid cells and protected epithelial barrier function. In p38α-deficient DCs, the TAK1–MKK4/7–JNK–c-Jun axis was hyperactivated, leading to high IL-27 levels, and inhibition of the JNK–c-Jun axis suppressed IL-27 expression. ChIP assay revealed direct binding of c-Jun to the promoter of Il27p28, which was further enhanced in p38α-deficient DCs. In summary, here we identify a key role for p38α signaling in DCs in regulating intestinal inflammatory response and tumorigenesis, and our finding may provide targets for the treatment of inflammatory intestinal diseases.


2020 ◽  
Vol 1 (1) ◽  
pp. 9-12
Author(s):  
Heru Purnomo ◽  
Mu'awanah Mu'awanah ◽  
Mohammad Nur Mudhofar

ABSTRACTBackground : Early mobilization is some effort to defend autonomy as early as possible by guiding the victim for defending fisiologis function (Carpenito, 2001).  According Smeltzer Bare (2002) in patient with colon inflammation disturbance, explained that change position encourage doing passive and active exercise to depend muscle and prevent tromboembolic.  Activity limitation changed suitable with daily necessary.  General anesthesia can cause decreasing colon movement with stimuli parasympatic obstruction in colon muscle.  Client with local anesthesia will experience same case.  Direction surgery which involved intestinal can cause stopping intestinal while movement. Surgery action with general anesthesia in RS.DR.R.Soeprapto Cepuoften was being done in juny – December 2012 period reported 166 cases.Objective : This study to determine the difference of early mobilization 6 hours and 8 hours toward intestine peristaltic on post operation patient with general anesthesia at RSUD dr. R. Soeprapto Cepu. Methods : Method of this research  used quasi eksperimental design and taking sampling method was stratified random sampling, research was done into 20 respondences.  Collecting data technique using observation technique.  Statistic analysis used Independent t-test exam, organize and data analysis with computer program assist SPSS for windows 16.Result : The result analysis was shown with independent t-test exam was be found t hitung 0,662, t table 2,101, p value 0,641.  Where is t hitung t table (0,662 2,101) and p value alpha (0,641 0,05) above can be conclude Ho was accepted.  Its mean its’nt difference early mobilization 6 hours and 8 hours about peristaltic of intestine for post operation patient with general anesthesia in dr.R.Soeprapto Cepu Hospitals.Conclusion : Advice we recommend early mobilization of patients immediately after surgery with general anesthesia, according to the results of this study was able to mobilize patients early in the post anesthesia 6 hours. Keywords: mobilisation, peristaltic of intestine, post operation, general anesthesia.


2018 ◽  
Vol 25 (1) ◽  
pp. 85-96 ◽  
Author(s):  
Margaret Delday ◽  
Imke Mulder ◽  
Elizabeth T Logan ◽  
George Grant

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