scholarly journals Modulation of Gut Barrier Functions in Ulcerative Colitis by Hyaluronic Acid System

2021 ◽  
pp. 2103189
Author(s):  
Niranjan G. Kotla ◽  
Isma Liza Mohd Isa ◽  
Swetha Rasala ◽  
Secil Demir ◽  
Rajbir Singh ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Hyaluronic Acid ◽  
Acid System ◽  
Gut Barrier ◽  
Barrier Functions

scholarly journals DNA‐Grafted Hyaluronic Acid System with Enhanced Injectability and Biostability for Photo‐Controlled Osteoarthritis Gene Therapy

2021 ◽  
pp. 2004793
Author(s):  
Zhijie Chen ◽  
Feng Zhang ◽  
Hongbo Zhang ◽  
Liang Cheng ◽  
Kaizhe Chen ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Hyaluronic Acid ◽  
Acid System

Changes in the hyaluronidase-hyaluronic acid system in the kidneys of rabbits with experimental intestitial nephritis

1964 ◽  
Vol 57 (3) ◽  
pp. 277-281
Author(s):  
A. G. Ginetsinskii ◽  
M. G. Zaks ◽  
V. I. Ioffe ◽  
T. V. Krestinskaya ◽  
M. M. Sokolova ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Acid System

Protective effects of Lizhong decoction on ulcerative colitis in mice by suppressing inflammation and ameliorating gut barrier

2020 ◽  
Vol 259 ◽  
pp. 112919 ◽  
Author(s):  
Yumeng Shen ◽  
Junfeng Zou ◽  
Mengjun Chen ◽  
Zhimiao Zhang ◽  
Chen Liu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Protective Effects ◽  
Gut Barrier

scholarly journals Mechanism of Ulcerative Colitis-Aggravated Liver Fibrosis: The Activation of Hepatic Stellate Cells and TLR4 Signaling Through Gut-Liver Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu-Feng Liu ◽  
Guo-Chao Niu ◽  
Chen-Yang Li ◽  
Jin-Bo Guo ◽  
Jia Song ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Liver Fibrosis ◽  
Bacterial Translocation ◽  
Hepatic Stellate Cells ◽  
Collagen Type ◽  
Stellate Cells ◽  
Gut Barrier ◽  
Tlr4 Signaling ◽  
Gut Barrier Function ◽  
Pro Inflammatory Cytokines

Background: The progression of liver disorders is frequently associated with inflammatory bowel disease through the gut-liver axis. However, no direct evidence showed the mechanisms of ulcerative colitis (UC) in the development of liver fibrosis per se. Thus, this study aimed to evaluate the effects of UC on liver fibrosis and its potential mechanism in the experimental model.Methods: Male C57BL/6 mice were allocated into five groups (n = 10 per group) to receive either drinking water (control), 2% dextran sulfate sodium (DSS), olive oil, carbon tetrachloride (CCl4) or DSS + CCl4 for 4 cycles. Blood was collected for biochemical analysis. Colons were excised for the evaluation of colon length and morphological score. Liver, colon, and mesenteric lymph nodes (MLNs) were collected for histopathological staining, expression analysis, and bacterial translocation assay to evaluate the inflammation, fibrosis, the activation of hepatic stellate cells (HSCs), and gut barrier function.Results: DSS caused severe colitis in mice treated or treated with CCl4, as evident from the elevation of disease activity index (DAI), histological abnormalities, and increased pro-inflammatory cytokines (TNF-α, IFN-γ, and IL-17A). Histopathological staining revealed that DSS treatment aggravated the CCl4-induced extracellular matrix deposition, liver fibrosis, and inflammation in mice. Additionally, biochemical and expression analysis indicated the DSS treatment caused the increase of hydroxyproline and pro-inflammatory cytokines, as well as the abnormal liver function indexes in CCl4-induced mice. Gut barrier function was impaired in DSS- and DSS + CCl4-treated mice, manifesting as the increase in bacterial translocation and lipopolysaccharide level, and the reduction in tight junction proteins (occluding, claudin-1 and ZO-1) expression. Further, the activations of HSCs and TLR4 signaling pathway were observed after DSS + CCl4 treatment, presenting with the increase in expression of α-SMA, vimentin, TGF-β, collagen type I, collagen type II, TIMP-2, TLR4, TRAF6, and NF-κB p65, and a decrease in GFAP and MMP-2 expression.Conclusion: The present study verified that UC aggravated CCl4-induced liver injury, inflammation, and fibrosis in mice through the gut-liver axis. Gut barrier dysfunction in UC leads to bacterial translocation and elevated lipopolysaccharide, which may promote the activation of TLR4 signaling and HSCs in the liver.

Gut microbiota-dependent catabolites of tryptophan play a predominant role in the protective effects of Turmeric polysaccharides against DSS-induced ulcerative colitis

2021 ◽  
Author(s):  
Chengcheng Yang ◽  
Yao Du ◽  
Daoyuan Ren ◽  
Xingbin Yang ◽  
Yan Zhao
Keyword(s):  
Ulcerative Colitis ◽  
Gut Microbiota ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Predominant Role ◽  
Gut Microbiota Dysbiosis

Gut barrier dysfunction is triggered by gut microbiota dysbiosis that is closely associated with ulcerative colitis. Here, we first studied the prophylactic capacity of turmeric polysaccharides (TPS) to ameliorate dextran...

scholarly journals The Hyaluronan-Related Genes HAS2, HYAL1-5, HYALP1 are Associated with Prognosis, Cell Viability and Spheroid Formation Capacity in Ovarian Cancer

2021 ◽  
Author(s):  
Jette Riecks ◽  
Balázs Győrffy ◽  
Ludwig Kiesel ◽  
Alberto Passi ◽  
Davide Vigetti ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hyaluronic Acid ◽  
Cell Viability ◽  
Cancer Patients ◽  
Cell Phenotype ◽  
Acid System ◽  
Hyaluronan Synthases ◽  
Response To Chemotherapy ◽  
The Impact

Abstract Purpose: Hyaluronan modulates tumor progression, including cell adhesion, cohesion, proliferation and invasion, and the cancer stem cell phenotype. In ovarian cancer, high levels of stromal hyaluronan are associated with poor prognosis. In this work hyaluronan synthases (HAS1-3) and hyaluronidases (HYAL1-5, HYALP1) were examined with regard to different levels of gene expression and its influence on ovarian cancer patients survival. The impact of a siRNA depletion of hyaluronic acid synthase HAS2 was investigated in vitro.Methods: Using the Kaplan Meier Plotter tool, we investigated the influence of hyaluronic synthesis enzymes on the survival of a collective of 1435 ovarian cancer patients. We studied SKOV3 ovarian cancer cells subjected to HAS2 siRNA or control siRNA treatment in terms of HAS1-3, HYAL2 and HYAL3 mRNA expression. We investigated the ability to form spheroids using the Hanging Drop method and the response to chemotherapy at different concentrations using the MTT Assay. By String analysis, interactions within the enzymes of the hyaluronic acid system and with binding partners were visualized. Results: HAS2 improves cell viability, the capability to form tumor spheroids and has a negative prognostic value regarding overall survival. Lower HAS2 expression and high expression of HYAL2 and HYAL3 favours the survival of ovarian cancer patients. HAS2 knockdown cells and control cells showed a moderate response to in vitro chemotherapy with Taxol, Cisplatin and combinatorial treatment. Conclusion: In conclusion our study shows that the hyaluronic acid system has a relevant influence on the survival of ovarian cancer patients and could therefore be considered as a possible prognostic factor.

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