Saccharomyces cerevisiae UFMG A-905 treatment reduces intestinal damage in a murine model of irinotecan-induced mucositis

2016 ◽  
Vol 7 (4) ◽  
pp. 549-557 ◽  
Author(s):  
R.W. Bastos ◽  
S.H.S.P. Pedroso ◽  
A.T. Vieira ◽  
L.M.C. Moreira ◽  
C.S. França ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Weight Loss ◽  
Post Treatment ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Intestinal Lesions ◽  
Probiotic Yeast ◽  
Indigenous Microbiota ◽  
Gastrointestinal Mucositis

Indigenous microbiota plays a crucial role in the development of several intestinal diseases, including mucositis. Gastrointestinal mucositis is a major and serious side effect of cancer therapy, and there is no effective therapy for this clinical condition. However, some probiotics have been shown to attenuate such conditions. To evaluate the effects of Saccharomyces cerevisiae UFMG A-905 (Sc-905), a potential probiotic yeast, we investigated whether pre- or post-treatment with viable or inactivated Sc-905 could prevent weight loss and intestinal lesions, and maintain integrity of the mucosal barrier in a mucositis model induced by irinotecan in mice. Only post-treatment with viable Sc-905 was able to protect mice against the damage caused by chemotherapy, reducing the weight loss, increase of intestinal permeability and jejunal lesions (villous shortening). Besides, this treatment reduced oxidative stress, prevented the decrease of goblet cells and stimulated the replication of cells in the intestinal crypts of mice with experimental mucositis. In conclusion, Sc-905 protects animals against irinotecan-induced mucositis when administered as a post-treatment with viable cells, and this effect seems to be related with the reduction of oxidative stress and preservation of intestinal mucosa.

scholarly journals Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

2020 ◽  
Author(s):  
Xiuhao Zhao ◽  
Jin Zhou ◽  
Wenhua Liang ◽  
Qingfeng Sheng ◽  
Li Lu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Necrotizing Enterocolitis ◽  
Animal Experiments ◽  
Intestinal Barrier ◽  
Pregnane X Receptor ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Jnk Pathway ◽  
Intestinal Lesions ◽  
Neonatal Necrotizing Enterocolitis

Abstract Background: Intestinal dysbiosis is believed to be one of the factors inducing neonatal necrotizing enterocolitis (NEC). Probiotics have been employed to treat NEC in a number of animal experiments and clinical trials, and some significant benefits of utilizing probiotics for the prevention or alleviation of NEC have been confirmed. However, the mechanism underlying the efficacy of probiotics in treating NEC has not been elucidated. Results: Impairment of the intestinal barrier, which was characterized by the decreased expression of tight junction components, was observed in the pathogenesis of NEC. The probiotic mixture alleviated this intestinal damage by enhancing the function of the barrier. Meanwhile, the probiotics remodeled the composition of the intestinal microbiota in NEC mice. Furthermore, increased expression of the pregnane X receptor ( PXR ) was observed after treatment with the probiotic mixture, and PXR overexpression in Caco-2 cells protected the barrier from lipopolysaccharide (LPS) damage. Further research showed that PXR could inhibit the phosphorylation of c-Jun N-terminal kinase (JNK) and could increase the expression of tight junction components. Conclusions: Our study confirmed that probiotics could ameliorate intestinal lesions by enhancing the function of the mucosal barrier. Specifically, probiotics may target PXR, which may subsequently enhance the expression of tight junction components by inhibiting the phosphorylation of JNK and enhancing the function of the barrier.

scholarly journals Low Molecular Seleno-Aminopolysaccharides Protect the Intestinal Mucosal Barrier of Rats under Weaning Stress

2019 ◽  
Vol 20 (22) ◽  
pp. 5727 ◽  
Author(s):  
Zheng-Shun Wen ◽  
Ming Du ◽  
Zhen Tang ◽  
Tian-Yi Zhou ◽  
Zhong-Shan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Intestinal Mucosa ◽  
Expression Level ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Intestinal Tissue ◽  
Intestinal Mucosal Barrier ◽  
Weaning Stress ◽  
Nrf2 Signaling Pathway

Low molecular seleno-aminopolysaccharide (LSA) was synthesized with sodium selenite and low molecular aminopolysaccharide (LA), which is an organic selenium compound. This study is aimed to investigate the protective effect of LSA on the intestinal mucosal barrier in weaning stress rats by detecting the intestinal tissue morphology and function, mucosal thickness and permeability, the structure of MUC2, antioxidant index, the expression level of intracellular transcription factor NF-E2-related factor 2 (Nrf2), and its related factors. The results showed that LSA significantly increased the height of intestinal villi (p < 0.05) and increased the thickness of intestinal mucosa and the number of goblet cells, which indicated that LSA has a protective effect on the intestinal mucosal barrier that is damaged by weaning. Moreover, LSA significantly reduced the level of DAO, D-LA, and LPS compared with the weaning group (p < 0.05), which indicated that LSA reduced the intestinal damage and permeability of weaning rats. In addition, LSA could increase the number and length of glycans chains and the abundance of acid glycans structures in the MUC2 structure, which indicated that LSA alleviated the changes of intestinal mucus protein structure. LSA significantly increased the levels of GSH-Px, SOD, LDH, and CAT, while it decreased the level of MDA in serum and intestinal tissue, which suggested that LSA significantly enhanced the antioxidant capacity and reduced oxidative stress of weaning rats. RT-PCR results showed that LSA significantly increased the expression level of antioxidant genes (GSH-Px, SOD, Nrf2, HO-1), glycosyltransferase genes (GalNT1, GalNT3, GalNT7) and mucin gene (MUC2) in intestinal mucosa (p < 0.05). The results of western blot showed that the LSA activated the Nrf2 signaling pathway by down-regulating the expression of Keap1and up-regulating the expression of Nrf2, and protected the intestinal mucosa from oxidative stress. Overall, LSA could play a protective role in intestinal mucosal barrier of weaning rats by activating the Nrf2 pathway and alleviating the alnormal change of mucin MUC2.

scholarly journals Probiotics mixture reinforces barrier function to ameliorate necrotizing enterocolitis by regulating PXR-JNK pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiuhao Zhao ◽  
Jin Zhou ◽  
Wenhua Liang ◽  
Qingfeng Sheng ◽  
Li Lu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Necrotizing Enterocolitis ◽  
Animal Experiments ◽  
Intestinal Barrier ◽  
Pregnane X Receptor ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Jnk Pathway ◽  
Intestinal Lesions ◽  
Neonatal Necrotizing Enterocolitis

Abstract Background Intestinal dysbiosis is believed to be one of the factors inducing neonatal necrotizing enterocolitis (NEC). Probiotics have been employed to treat NEC in a number of animal experiments and clinical trials, and some significant benefits of utilizing probiotics for the prevention or alleviation of NEC have been confirmed. However, the mechanism underlying the efficacy of probiotics in treating NEC has not been elucidated. Results Impairment of the intestinal barrier, which was characterized by the decreased expression of tight junction components, was observed in the pathogenesis of NEC. The probiotic mixture alleviated this intestinal damage by enhancing the function of the barrier. Meanwhile, the probiotics remodeled the composition of the intestinal microbiota in NEC mice. Furthermore, increased expression of the pregnane X receptor (PXR) was observed after treatment with the probiotic mixture, and PXR overexpression in Caco-2 cells protected the barrier from lipopolysaccharide (LPS) damage. Further research showed that PXR could inhibit the phosphorylation of c-Jun N-terminal kinase (JNK) and could increase the expression of tight junction components. Conclusions Our study confirmed that probiotics could ameliorate intestinal lesions by enhancing the function of the mucosal barrier. Specifically, probiotics may target PXR, which may subsequently enhance the expression of tight junction components by inhibiting the phosphorylation of JNK and enhance the function of the barrier.

scholarly journals Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

2020 ◽  
Author(s):  
Xiuhao Zhao ◽  
Jin Zhou ◽  
Wenhua Liang ◽  
Qingfeng Sheng ◽  
Li Lu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Necrotizing Enterocolitis ◽  
Animal Experiments ◽  
Intestinal Barrier ◽  
Pregnane X Receptor ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Jnk Pathway ◽  
Intestinal Lesions ◽  
Neonatal Necrotizing Enterocolitis

Abstract Background: Intestinal dysbiosis is believed to be one of the factors inducing neonatal necrotizing enterocolitis (NEC). Probiotics have been employed to treat NEC in a number of animal experiments and clinical trials, and some significant benefits of utilizing probiotics for the prevention or alleviation of NEC have been confirmed. However, the mechanism underlying the efficacy of probiotics in treating NEC has not been elucidated.Results: Impairment of the intestinal barrier, which was characterized by the decreased expression of tight junction components, was observed in the pathogenesis of NEC. The probiotic mixture alleviated this intestinal damage by enhancing the function of the barrier. Meanwhile, the probiotics remodeled the composition of the intestinal microbiota in NEC mice. Furthermore, increased expression of the pregnane X receptor (PXR) was observed after treatment with the probiotic mixture, and PXR overexpression in Caco-2 cells protected the barrier from lipopolysaccharide (LPS) damage. Further research showed that PXR could inhibit the phosphorylation of c-Jun N-terminal kinase (JNK) and could increase the expression of tight junction components.Conclusions: Our study confirmed that probiotics could ameliorate intestinal lesions by enhancing the function of the mucosal barrier. Specifically, probiotics may target PXR, which may subsequently enhance the expression of tight junction components by inhibiting the phosphorylation of JNK and enhancing the function of the barrier.

scholarly journals Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

2021 ◽  
Author(s):  
Xiuhao Zhao ◽  
Jin Zhou ◽  
Wenhua Liang ◽  
Qingfeng Sheng ◽  
Li Lu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Necrotizing Enterocolitis ◽  
Animal Experiments ◽  
Intestinal Barrier ◽  
Pregnane X Receptor ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Jnk Pathway ◽  
Intestinal Lesions ◽  
Neonatal Necrotizing Enterocolitis

Abstract Background: Intestinal dysbiosis is believed to be one of the factors inducing neonatal necrotizing enterocolitis (NEC). Probiotics have been employed to treat NEC in a number of animal experiments and clinical trials, and some significant benefits of utilizing probiotics for the prevention or alleviation of NEC have been confirmed. However, the mechanism underlying the efficacy of probiotics in treating NEC has not been elucidated.Results: Impairment of the intestinal barrier, which was characterized by the decreased expression of tight junction components, was observed in the pathogenesis of NEC. The probiotic mixture alleviated this intestinal damage by enhancing the function of the barrier. Meanwhile, the probiotics remodeled the composition of the intestinal microbiota in NEC mice. Furthermore, increased expression of the pregnane X receptor (PXR) was observed after treatment with the probiotic mixture, and PXR overexpression in Caco-2 cells protected the barrier from lipopolysaccharide (LPS) damage. Further research showed that PXR could inhibit the phosphorylation of c-Jun N-terminal kinase (JNK) and could increase the expression of tight junction components.Conclusions: Our study confirmed that probiotics could ameliorate intestinal lesions by enhancing the function of the mucosal barrier. Specifically, probiotics may target PXR, which may subsequently enhance the expression of tight junction components by inhibiting the phosphorylation of JNK and enhancing the function of the barrier.

Oxidative stress does not influence weight loss induced by aerobic training in adults: randomized clinical trials

2020 ◽  
Vol 60 (6) ◽  
Author(s):  
Glêbia A. Cardoso ◽  
Mateus D. Ribeiro ◽  
Ana P. Ferreira ◽  
Yohanna de Oliveira ◽  
Thiago de O. Medeiros ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Weight Loss ◽  
Clinical Trials ◽  
Randomized Clinical Trials ◽  
Aerobic Training

Idebenone Treatment Mediates the Effect of Menadione Oxidative Stress Damage in Saccharomyces cerevisiae

2012 ◽  
Vol 6 (2) ◽  
pp. 120-123 ◽  
Author(s):  
Oliver Gamondi ◽  
Sebastian Chapela ◽  
Ines Nievas ◽  
Isabel Burgos ◽  
Manuel Alonso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Stress Damage

Food antigens exacerbate intestinal damage and inflammation following the disruption of the mucosal barrier

2021 ◽  
Vol 96 ◽  
pp. 107670
Author(s):  
Yanmei Ma ◽  
Zhihua Yin ◽  
Li Li ◽  
Bingni Chen ◽  
Hanying Dai ◽  
...  
Keyword(s):  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Food Antigens

Short-term Effects of Metformin on Cardiac and Peripheral Blood Cells Following Cecal Ligation and Puncture-induced Sepsis

Drug Research ◽  
2020 ◽  
Author(s):  
Tina Didari ◽  
Shokoufeh Hassani ◽  
Maryam Baeeri ◽  
Mona Navaei-Nigjeh ◽  
Mahban Rahimifard ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Weight Loss ◽  
Blood Cells ◽  
Cell Injury ◽  
Antioxidant Properties ◽  
Cecal Ligation ◽  
Neutrophil Infiltration ◽  
Cardiac Cells ◽  
Cecal Ligation And Puncture ◽  
Blood Profile

Abstract Aim of the study Sepsis has well-documented inflammatory effects on cardiovascular and blood cells. This study is designed to investigate potential anti-inflammatory effects of metformin on cardiac and blood cells 12 and 24 h following cecal ligation and puncture (CLP)-induced sepsis. Methods For the purpose of this study, 36 male Wistar rats were divided into six groups: two groups underwent CLP, two groups underwent CLP and received metformin, and two groups only received sham operations. 12 h later, 18 rats (half of rats in each of the three aforementioned groups) were sacrificed and cardiac and blood cells were harvested. Subsequently, 12 h later, the rest of the rats were euthanatized. In all harvested blood and cardiac cells, oxidative stress indicators, antioxidant properties, count of blood cells, neutrophil infiltration, percentage of weight loss and pathological assessment were conducted. Results In our experiment, metformin elevated antioxidant levels, improved function of blood cells and percentage of weight loss. Moreover, in the groups which received metformin, oxidative stress and neutrophil infiltration markers were decreased significantly. Moreover, pathological investigations of cardiac cell injury were reduced in the metformin group. Conclusions Our findings suggest that in CLP induced sepsis model, metformin can improve the function of blood and cardiac cells through alleviating inflammation, improvement of anti-inflammation properties, and enhancement of blood profile, and all these effects are more pronounced after 24 h in comparison with 12 h after induction of sepsis.

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