scholarly journals Polysaccharides extracted from Rheum tanguticum ameliorate radiation-induced enteritis via activation of Nrf2/HO-1

2020 ◽  
Vol 62 (1) ◽  
pp. 46-57
Author(s):  
Tian Zhang ◽  
Lei Shi ◽  
Yan Li ◽  
Wei Mu ◽  
HaoMeng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Early Stage ◽  
Underlying Mechanism ◽  
Intestinal Injury ◽  
Inflammatory Factors ◽  
Multiple Time ◽  
Intestinal Damage ◽  
Time Points ◽  
Radiation Induced ◽  
Rheum Tanguticum

ABSTRACT Radiation-induced enteritis is a major side effect in cancer patients undergoing abdominopelvic radiotherapy. The Nrf2/HO-1 pathway is a critical endogenous antioxidant stress pathway, but its precise role in radiation-induced enteritis remains to be clarified. Polysaccharides extracted from Rheum tanguticum (RTP) can protect the intestinal cells from radiation-induced damage, but the underlying mechanism is unknown. SD rats and IEC-6 cells were exposed to 12 or 10 Gy X-ray radiation. Rat survival, and histopathological and immunohistochemical profiles were analyzed at different time points. Indicators of oxidative stress and inflammatory response were also assessed. Cell viability, apoptosis and Nrf2/HO-1 expression were evaluated at multiple time points. Significant changes were observed in the physiological and biochemical indexes of rats after radiation, accompanied by significant oxidative stress response. The mRNA and protein expression of Nrf2 peaked at 12 h after irradiation, and HO-1 expression peaked at 48 h after irradiation. RTP administration reduced radiation-induced intestinal damage, upregulated Nrf2/HO-1, improved physiological indexes, significantly decreased apoptosis and inflammatory factors, and upregulated HO-1, particularly at 48 h after irradiation. In conclusion, Nrf2 is activated in the early stage of radiation-induced intestinal injury and plays a protective role. RTP significantly ameliorates radiation-induced intestinal injury via the regulation of Nrf2 and its downstream protein HO-1.

scholarly journals Heme Oxygenase-1-Mediated Autophagy Protects against Oxidative Damage in Rat Nucleus Pulposus-Derived Mesenchymal Stem Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Sheng Chen ◽  
Sheng Liu ◽  
Lei Zhao ◽  
Hui Lin ◽  
Kaige Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cell Viability ◽  
Nucleus Pulposus ◽  
Heme Oxygenase ◽  
Early Stage ◽  
Underlying Mechanism ◽  
Research Direction ◽  
Heme Oxygenase 1 ◽  
Ivd Degeneration

Although endogenous nucleus pulposus-derived mesenchymal stem cell- (NPMSC-) based regenerative medicine has provided promising repair strategy for intervertebral disc (IVD) degeneration, the hostile microenvironments in IVD, including oxidative stress, can negatively affect the survival and function of the NPMSCs and severely hinder the endogenous repair process. Therefore, it is of great importance to reveal the mechanisms of the endogenous repair failure caused by the adverse microenvironments in IVD. The aim of this study was to investigate the effect of oxidative stress on the rat NPMSCs and its underlying mechanism. Our results demonstrated that oxidative stress inhibited cell viability, induced apoptosis, and increased the production of reactive oxygen species (ROS) in NPMSCs. In addition, the results showed that the expression level of heme oxygenase-1 (HO-1) increased at an early stage but decreased at a late stage when NPMSCs were exposed to oxidative stress, and the oxidative damages of NPMSCs could be partially reversed by promoting the expression of HO-1. Further mechanistic analysis indicated that the protective effect of HO-1 against oxidative damage in NPMSCs was mediated by the activation of autophagy. Taken together, our study revealed that oxidative stress could inhibit cell viability, induce apoptosis, and increase ROS production in NPMSCs, and HO-1-mediated autophagy might act as a protective response to the oxidative damage. These findings might enhance our understanding on the mechanism of the endogenous repair failure during IVD degeneration and provide novel research direction for the endogenous repair of IVD degeneration.

p-Coumaric acid ameliorates ionizing radiation-induced intestinal injury through modulation of oxidative stress and pyroptosis

Life Sciences ◽  
2021 ◽  
Vol 278 ◽  
pp. 119546
Author(s):  
Yun-Hong Li ◽  
Qian He ◽  
Yu-Zhong Chen ◽  
Ya-Fang Du ◽  
Ya-Xin Guo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ionizing Radiation ◽  
Intestinal Injury ◽  
Coumaric Acid ◽  
Radiation Induced

scholarly journals C/EBPδ protects from radiation-induced intestinal injury and sepsis by suppression of inflammatory and nitrosative stress

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sudip Banerjee ◽  
Qiang Fu ◽  
Sumit K. Shah ◽  
Stepan B Melnyk ◽  
Esta Sterneck ◽  
...  
Keyword(s):  
Nitrosative Stress ◽  
Intestinal Barrier ◽  
Intestinal Injury ◽  
Nuclear Antigen ◽  
Intestinal Damage ◽  
Oxidative And Nitrosative Stress ◽  
Tnf Α ◽  
Radiation Induced ◽  
Villous Height ◽  
Proliferating Cell

Abstract Ionizing radiation (IR)-induced intestinal damage is characterized by a loss of intestinal crypt cells, intestinal barrier disruption and translocation of intestinal microflora resulting in sepsis-mediated lethality. We have shown that mice lacking C/EBPδ display IR-induced intestinal and hematopoietic injury and lethality. The purpose of this study was to investigate whether increased IR-induced inflammatory, oxidative and nitrosative stress promote intestinal injury and sepsis-mediated lethality in Cebpd−/− mice. We found that irradiated Cebpd−/− mice show decreased villous height, crypt depth, crypt to villi ratio and expression of the proliferation marker, proliferating cell nuclear antigen, indicative of intestinal injury. Cebpd−/− mice show increased expression of the pro-inflammatory cytokines (Il-6, Tnf-α) and chemokines (Cxcl1, Mcp-1, Mif-1α) and Nos2 in the intestinal tissues compared to Cebpd+/+ mice after exposure to TBI. Cebpd−/− mice show decreased GSH/GSSG ratio, increased S-nitrosoglutathione and 3-nitrotyrosine in the intestine indicative of basal oxidative and nitrosative stress, which was exacerbated by IR. Irradiated Cebpd-deficient mice showed upregulation of Claudin-2 that correlated with increased intestinal permeability, presence of plasma endotoxin and bacterial translocation to the liver. Overall these results uncover a novel role for C/EBPδ in protection against IR-induced intestinal injury by suppressing inflammation and nitrosative stress and underlying sepsis-induced lethality.

scholarly journals The influence on oxidative stress markers, inflammatory factors and intestinal injury-related molecules in Wahui pigeon induced by lipopolysaccharide

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0251462
Author(s):  
Fei Wang ◽  
Jin Liu ◽  
Xiaofen Hu ◽  
Youbao Zhong ◽  
Feng Wen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mrna Expression ◽  
Histopathological Examination ◽  
Intestinal Injury ◽  
Inflammatory Factors ◽  
Control Group ◽  
Inflammatory Factor ◽  
Expression Levels ◽  
Lps Challenge ◽  
Mrna Expression Levels

Introduction The intestinal structure is the foundation for various activities and functions in poultry. An important question concerns the changes in the intestinal status under endotoxin stimulation. This study aimed to investigate the mechanism of intestinal injury induced by lipopolysaccharide (LPS) in Wahui pigeons. Methods Thirty-six 28-day-old healthy Wahui pigeons were randomly divided into two groups. The experimental group was injected with LPS (100 μg/kg) once per day for five days, and the control group was treated with the same amount of sterile saline. Blood and the ileum were collected from pigeons on the first, third, and fifth days of the experiment and used for oxidative stress assessment, inflammatory factor detection, histopathological examination, and positive cell localization. In addition, intestinal injury indices and mRNA expression levels (tight junction proteins, inflammatory cytokines, and factors related to autophagy and apoptosis) were evaluated. Results Villi in the ileum were shorter in the LPS group than in the control group, and D-lactic acid levels in the serum were significantly increased. Glutathione and catalase levels significantly decreased, but the malondialdehyde content in the serum increased. TNF-α and IL-10 were detected at higher levels in the serum, with stronger positive signals and higher mRNA expression levels, in the LPS group than in the control group. In addition, the levels of TLR4, MyD88, NF-κB, and HMGB1 in the inflammatory signaling pathway were also upregulated. Finally, the mRNA expression of Claudin3, Occludin, and ZO-1 was significantly decreased; however, that of Beclin1 and Atg5 was increased in the LPS group. Conclusion Ileal pathological changes and oxidative stress were caused by LPS challenge; it is proposed that this triggering regulates the inflammatory response, causing excessive autophagy and apoptosis, promoting intestinal permeability, and leading to intestinal injury in Wahui pigeons.

Weight change among breast cancer patients receiving chemotherapy: A retrospective analysis

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 19535-19535
Author(s):  
B. P. Nair ◽  
O. Khalil ◽  
V. R. Phooshkooru ◽  
L. F. Hutchins
Keyword(s):  
Breast Cancer ◽  
Weight Gain ◽  
Cancer Patients ◽  
Early Stage ◽  
Entire Population ◽  
Multiple Time ◽  
Age Group ◽  
Breast Cancer Patients ◽  
Time Points ◽  
The Mean

19535 Background: Weight gain occurs in patients with early stage breast cancer receiving chemotherapy. The etiology is unknown. Most pre-menopausal patients receiving chemotherapy enter menopause during the course of treatment. We explored the relation between weight gain and development of menopause in breast cancer patients. We hypothesized that, among breast cancer patients receiving chemotherapy, those in the pre/perimenopausal group will gain more weight compared to postmenopausal group in the first 2 years. Methods: The electronic database at University of Arkansas was queried for breast cancer patients treated with chemotherapy between May 1992 and Nov 2003. Age, chemotherapy and weight at multiple time points (diagnosis, 6, 12, 24 and 60 months) were obtained. The mean weight changes across these time points were then calculated for the entire population and also after categorizing by age. Age was used as a surrogate for menstrual status. Women aged >=50 yrs were considered postmenopausal, those <50 yrs were considered pre or perimenopausal. Results: 617 patients were included in the analysis. There were 371 patients in the >=50 age group and 246 patients in the <50 age group. The average baseline weight for the entire population was 75.21 kg: 74.44 for women <50 yrs and 75.71 for women >= 50 yrs. Patients <50 yrs of age gained weight in the first 2 yrs: 1.11 kg weight in the 1st year and 0.65 kg in the second yr. This was followed by loss of 1.19 kg over next 3 yrs which paralleled the loss of weight in the >=50 group. The mean weight of the >=50 age decreased by 0.27 kg in the first 2 years and then by 1.16 kg over the next 3 yrs following chemotherapy. Conclusions: Pre/perimenopausal breast cancer patients in our study gained weight, while postmenopausal patients had slight weight loss during the first 2 years. These findings imply that onset of menopause itself may be playing a significant role in weight gain among pre/perimenopausal breast cancer patients receiving chemotherapy. [Table: see text] No significant financial relationships to disclose.

(−)-Epicatechin mitigates radiation-induced intestinal injury and promotes intestinal regeneration via suppressing oxidative stress

2019 ◽  
Vol 53 (8) ◽  
pp. 851-864 ◽  
Author(s):  
Ya Li ◽  
Shanshan Ma ◽  
Yanting Zhang ◽  
Minghao Yao ◽  
Xiangzhan Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Injury ◽  
Intestinal Regeneration ◽  
Radiation Induced

scholarly journals Protective effects of seabuckthorn pulp and seed oils against radiation-induced acute intestinal injury

2017 ◽  
Vol 58 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Jing Shi ◽  
Lan Wang ◽  
Yan Lu ◽  
Yue Ji ◽  
Yaqing Wang ◽  
...  
Keyword(s):  
Map Kinases ◽  
Seed Oil ◽  
Intestinal Injury ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Inflammatory Factors ◽  
High Dose ◽  
Seed Oils ◽  
Protective Effects ◽  
Radiation Induced ◽  
Post Radiation

Abstract Radiation-induced gastrointestinal syndrome, including nausea, diarrhea and dehydration, contributes to morbidity and mortality after medical or industrial radiation exposure. No safe and effective radiation countermeasure has been approved for clinical therapy. In this study, we aimed to investigate the potential protective effects of seabuckthorn pulp and seed oils against radiation-induced acute intestinal injury. C57/BL6 mice were orally administered seabuckthorn pulp oil, seed oil and control olive oil once per day for 7 days before exposure to total-body X-ray irradiation of 7.5 Gy. Terminal deoxynucleotidyl transferase dUTP nick end labeling, quantitative real-time polymerase chain reaction and western blotting were used for the measurement of apoptotic cells and proteins, inflammation factors and mitogen-activated protein (MAP) kinases. Seabuckthorn oil pretreatment increased the post-radiation survival rate and reduced the damage area of the small intestine villi. Both the pulp and seed oil treatment significantly decreased the apoptotic cell numbers and cleaved caspase 3 expression. Seabuckthorn oil downregulated the mRNA level of inflammatory factors, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6 and IL-8. Both the pulp and seed oils elevated the level of phosphorylated extracellular-signal-regulated kinase and reduced the levels of phosphorylated c-Jun N-terminal kinase and p38. Palmitoleic acid (PLA) and alpha linolenic acid (ALA) are the predominant components of pulp oil and seed oil, respectively. Pretreatment with PLA and ALA increased the post-radiation survival time. In conclusion, seabuckthorn pulp and seed oils protect against mouse intestinal injury from high-dose radiation by reducing cell apoptosis and inflammation. ALA and PLA are promising natural radiation countermeasure candidates.

scholarly journals Anti-Oxidative and Immuno-Protective Effect of Camel Milk on Radiation-Induced Intestinal Injury in C57BL/6 J Mice

Dose-Response ◽  
2021 ◽  
Vol 19 (1) ◽  
pp. 155932582110037
Author(s):  
Yu-Zhong Chen ◽  
Chao Li ◽  
Jia Gu ◽  
Si-chen Lv ◽  
Jia-ying Song ◽  
...  
Keyword(s):  
Survival Rate ◽  
Protective Effect ◽  
Survival Time ◽  
Intestinal Injury ◽  
Camel Milk ◽  
Whole Body ◽  
Inflammatory Factors ◽  
Control Group ◽  
Irradiation Group ◽  
Radiation Induced

Purpose: The main objective is to investigate the protective effect of camel milk (CM) on radiation-induced intestinal injury. Methods: The C57BL/6 J mice in 2 experiments were assigned into control group (Con), irradiation group (IR), and CM+irradiation group (CM+IR). After receiving the CM via gavage for 14 days, the mice in the first experiment were exposed to 6 Gy X-ray whole body irradiation, and survival rate was compared among the groups. Mice in the second experiment were exposed to 4 Gy irradiation and sacrificed at day 7. The small intestines were collected to examine the histopathological changes and to determine the anti-oxidative index and HMGB1/TLR4 inflammatory pathway. Fasting blood was used to measure serum pro-inflammatory factors. Results: Compared with the IR group, the survival time was prolonged, and survival rate was increased in the CM+IR group. CM increased levels of SOD and GSH and decreased MDA in the jejunum. Furthermore, intestinal protein expression of HMGB1/TLR4 pathway (TLR4, NF-κB, and HMGB1) was up-regulated by CM intervention. CM decreased the serum levels of TNF-α and IL-1β and increased IL-10 level. Conclusions: CM extended the survival time and had a protective effect against radiation-induced jejunum injury by regulation of antioxidant capacity and HMGB1/TLR4/NF-κB/MyD88 inflammatory signaling pathway.

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