Effect of Vitamin E Supplementation on Intestinal Barrier Function in Rats Exposed to High Altitude Hypoxia Environment

Xu, Chunlan; Sun, Rui; Qiao, Xiangjin; Xu, Cuicui; Shang, Xiaobing; Niu, Weining; Chao, Yu–Faye

doi:10.4196/kjpp.2014.18.4.313

Cited by 31 publications

(18 citation statements)

References 44 publications

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“…The damage of intestinal mucosal barrier caused by burn is related to the intestinal oxidative stress injury and lipid peroxidation (Yalcin et al, 2012; Xu et al, 2014; Cheng et al, 2017) . MDA can reflect the degree of lipid peroxidation in the body and damage degree of cells under oxidative stress (Martinez Aranzales et al, 2015) .…”

Section: Discussionmentioning

confidence: 99%

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

Bian

Liu

et al. 2019

Mol Med

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BackgroundIntestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients. The current study established a burn model in rats and used a free radical scavenger edaravone (ED) to treat the rats, so as to investigate the effect of edaravone on intestinal mucosa barrier after burn injury.MethodsAnesthetized rats were subjected to 40% total body surface area water burn immediately, followed by treatment with ED, scrambled antagomir, or antagomiR-320. Intestinal mucosa damage was observed by hematoxylin-eosin staining and graded by colon mucosal damage index (CMDI) score. The contents of total sulfhydryl (TSH), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were determined by spectrophotometry. Cell apoptosis, protein relative expression,and the in situ expressions of p-Akt and p-Bad were detected by flow cytometry, Western blotting and immunohistochemistry, respectively. The miR-320 expression was determined by quantitative real-time polymerase chain reaction.ResultsED alleviated intestinal mucosal damage caused by burn injury, down-regulated the levels of MDA, cytochrome C, cleaved caspase-9 and cleaved caspase-3, but up-regulated the levels of TSH, SOD, CAT and Bcl-2. We also found that ED could reduce oxidative stress, inhibit cell apoptosis, increase the expressions of p-Akt, p-Bad and miR-320, and decrease PTEN expression. PTEN was predicted to be the target gene for miR-320, and cell apoptosis could be promoted by inhibiting miR-320 expression.ConclusionED regulates Akt/Bad/Caspase signaling cascade to reduce apoptosis and oxidative stress through up-regulating miR-320 expression and down-regulating PTEN expression, thus protecting the intestinal mucosal barrier of rats from burn injury.

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Section: Discussionmentioning

confidence: 99%

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

Bian

Liu

et al. 2019

Mol Med

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“…The anti-inflammatory effect of CO is perhaps the most intriguing therapeutic application. Inflammation is involved in a variety of pathologies in response to acute stress, including hypobaric hypoxia [10]. In inflammatory animal models, CO reduces the production of proinflammatory cytokines and prevents endothelial cell apoptosis [11,12,13].…”

Section: Introductionmentioning

confidence: 99%

Carbon Monoxide-Saturated Hemoglobin-Based Oxygen Carriers Attenuate High-Altitude-Induced Cardiac Injury by Amelioration of the Inflammation Response and Mitochondrial Oxidative Damage

Wang

Hu²,

Hu³

et al. 2016

Cardiology

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Objective: To investigate the therapeutic effect of carbon monoxide (CO) on high-altitude hypoxia-induced cardiac damage. Methods: Forty male C57BL/6 mice were randomly divided into 4 groups. The mice were exposed to normoxia or simulated 5,500-meter high-altitude hypoxia in a hypobaric chamber for 7 days. During the first 3 days, the mice were pretreated with CO-saturated hemoglobin (Hb)-based oxygen carrier (CO-HBOC), oxygen-saturated hemoglobin-based oxygen carrier (O₂-HBOC) at a dose of 0.3 g Hb/kg/day or an equivalent volume of saline. The in vivo left ventricle function, cardiac enzyme release, histopathological changes, apoptosis and inflammation were also measured. Results: High-altitude hypoxia induced significant cardiac damage, as demonstrated by impaired cardiac function and increased proapoptotic, proinflammatory and pro-oxidant markers. Pretreatment with CO-HBOC significantly improved cardiac performance, reduced cardiac enzyme release and limited myocardial apoptosis. The increased inflammatory response was also suppressed. In addition to the preserved mitochondrial structure, hypobaric hypoxia-induced mitochondrial oxidative damage was remarkably attenuated. Moreover, these antiapoptotic and antioxidative effects were accompanied by an upregulated phosphorylation of Akt, ERK and STAT3. Conclusion: This study demonstrated that CO-HBOC provides a promising protective effect on high-altitude hypoxia-induced myocardial injury, which is mediated by the inhibition of inflammation and mitochondrial oxidative damage.

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“…Apart from probiotics and polyphenols, other dietary components and food-derived chemicals by microbiota are suggested to pose positive effects on intestinal barrier function. Vitamins are potent antioxidants: it was shown that dietary supplementation with vitamin E ameliorated hypoxia-induced intestinal damage in rats (Xu et al 2014). Also, in a double-blind trial conducted in Brazil, children prescribed with vitamin A, zinc and glutamine showed improved intestinal barrier function, possibly via interaction with leptin (Lima et al 2014).…”

Section: Other Dietary Components and Food-derived Chemicalsmentioning

confidence: 99%

Influence of functional food components on gut health

Wan

Ling

El-Nezami

et al. 2018

Critical Reviews in Food Science and Nutrition

125

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Intestinal epithelial cells (IECs) lining the gastrointestinal tract establish a barrier between external environments and the internal milieu. An intact intestinal barrier maintains gut health and overall good health of the body by preventing from tissue injury, pathogen infection and disease development. When the intestinal barrier function is compromised, bacterial translocation can occur. Our gut microbiota also plays a fundamentally important role in health, for example, by maintaining intestinal barrier integrity, metabolism and modulating the immune system, etc. Any disruption of gut microbiota composition (also termed dysbiosis) can lead to various pathological conditions. In short, intestinal barrier and gut microbiota are two crucial factors affecting gut health. The gastrointestinal tract is a complex environment exposed to many dietary components and commensal bacteria. Dietary components are increasingly recognized to play various beneficial roles beyond basic nutrition, resulting in the development of the functional food concepts. Various dietary modifiers, including the consumption of live bacteria (probiotics) and ingestible food constituents such as prebiotics, as well as polyphenols or synbiotics (combinations of probiotics and prebiotics) are the most well characterized dietary bioactive compounds and have been demonstrated to beneficially impact the gut health and the overall well-being of the host. In this review we depict the roles of intestinal epithelium and gut microbiota in mucosal defence responses and the influence of certain functional food components on the modulation of gut health, with a particular focus on probiotics, prebiotics and polyphenols.

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Effect of Vitamin E Supplementation on Intestinal Barrier Function in Rats Exposed to High Altitude Hypoxia Environment

Cited by 31 publications

References 44 publications

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

Edaravone reduces oxidative stress and intestinal cell apoptosis after burn through up-regulating miR-320 expression

Carbon Monoxide-Saturated Hemoglobin-Based Oxygen Carriers Attenuate High-Altitude-Induced Cardiac Injury by Amelioration of the Inflammation Response and Mitochondrial Oxidative Damage

Influence of functional food components on gut health

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