scholarly journals Probiotic Bacillus Attenuates Oxidative Stress- Induced Intestinal Injury via p38-Mediated Autophagy

2019 ◽  
Vol 10 ◽  
Author(s):  
Yanping Wu ◽  
Baikui Wang ◽  
Han Xu ◽  
Li Tang ◽  
Yali Li ◽  
...  
2019 ◽  
Vol 97 (3) ◽  
pp. 193-196 ◽  
Author(s):  
Bo Li ◽  
Fang Zhou Yu ◽  
Adam Minich ◽  
Alison Hock ◽  
Carol Lee ◽  
...  

Maternal separation (MS) is a well-studied phenomenon thought to play a role in the pathogenesis of many diseases ranging from neuropsychiatric to early intestinal disorders such as necrotizing enterocolitis. The existing evidence suggests that MS initiates a variety of processes that in turn lead to early intestinal injury. Although there are many theories as to how MS alters normal physiological processes, the exact mechanism of action remains to be elucidated. This review aims to describe some of the pathological processes affecting the intestine that are caused by MS, including (i) brain–gut axis, (ii) intestinal epithelial barrier function, (iii) microbiome, (iv) oxidative stress and endoplasmic reticulum stress, and (v) gut inflammation.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiao-hong Du ◽  
Qing-jun Chen ◽  
Jian-bo Song ◽  
Yan Xie ◽  
Yan Zhi ◽  
...  

Rhubarb-Aconite Decoction (RAD), a famous Chinese medicine prescription, has been widely used for treating intestinal injury. However, the effect of RAD on intestinal epithelial cells is unclear. The aim of this study was to investigate the effects of RAD drug-containing serum on the oxidative stress injury and inflammatory response induced by endotoxin (ET) in Caco-2 cells in vitro. Lipid peroxide malondialdehyde (MDA), lactate dehydrogenase (LDH), caspase-11, tumor necrosis factor-α(TNF-α), interleukin-3(IL-3), and cytokeratin (CK)18, adenosine triphosphate (ATP) activity, and intracellular free calcium ion levels were measured. The results showed that ET triggered the activation of caspase-11 and the massive release of TNF-α, increased the inhibitory rate of cell growth, MDA, and LDH expressions in Caco-2 cells. Moreover, RAD drug-containing serum could inhibit caspase-11 activation, decrease the release of TNF-α and IL-3, reduce intracellular free calcium ion, and enhance CK 18 expression and ATP activity. These novel findings demonstrated that ET-induced oxidative stress injury and inflammatory response of Caco-2 cells were improved by RAD drug-containing serum, indicating that RAD may be a good choice for the treatment of intestinal injury.


2020 ◽  
Vol 10 (5) ◽  
pp. 669-675
Author(s):  
Junzhi Pan ◽  
Jie Zhang

Intestinal injury caused by sepsis has multiple effects on the pathophysiology and development of sepsis. In this study, we aimed to explore the role of FNDC5 in progression of sepsis-induced intestinal injury. The expression of FNDC5 in blood samples of patients with sepsis-induced intestinal injury and IEC-6 cells was measured by qRT-PCR assay. Cell viability and inflammatory cytokines were evaluated by CCK-8 and ELISA assay, respectively. Oxidative stress level was detected by DCFH-DA staining and corresponding kit. Tunel assay and western blot analysis were performed to assess cell apoptosis. FNDC5 expression in patients with sepsis-induced intestinal injury was significantly decreased. The stimulation of LPS reduced expression level of FNDC5 and inhibited cell growth in IEC-6 cells. Overexpression of FNDC5 suppressed the productions of TNF-a, IL-1 , IL-6 and MCP1, diminished the level of ROS and MPO while enhanced the SOD activity. Additionally, upregulation of FNDC5 ameliorated cell apoptosis and repressed the levels of apoptosis-related proteins. FNDC5 could play a crucial role in the inflammation, oxidative stress and apoptosis in sepsis-induced intestinal injury.


Life Sciences ◽  
2021 ◽  
Vol 278 ◽  
pp. 119546
Author(s):  
Yun-Hong Li ◽  
Qian He ◽  
Yu-Zhong Chen ◽  
Ya-Fang Du ◽  
Ya-Xin Guo ◽  
...  

2021 ◽  
Vol 105 (4) ◽  
pp. 1657-1668
Author(s):  
Lihong Hao ◽  
Yuanzhi Cheng ◽  
Weifa Su ◽  
Cheng Wang ◽  
Zeqing Lu ◽  
...  

2020 ◽  
Vol 62 (1) ◽  
pp. 46-57
Author(s):  
Tian Zhang ◽  
Lei Shi ◽  
Yan Li ◽  
Wei Mu ◽  
HaoMeng Zhang ◽  
...  

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.


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