200 mM hypertonic saline resuscitation attenuates intestinal injury and inhibits p38 signaling in rats after severe burn trauma

Sun, Yexiang; Han, Li-Nian; Zhi, Guang; Wu, Xue-Sheng; Zhou, Min; Wang, Fei; Peszel, April; Chen, Xulin

doi:10.1016/j.burns.2017.04.013

Cited by 9 publications

(5 citation statements)

References 54 publications

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“…Thermal burn injury is a leading cause of mortality and disability worldwide (21,22). Previous studies support the existence of intestinal injury following severe burn in rats (23,24). Histopathological examination in the present study further suggested that the intestinal tissues were noticeably damaged at 24 h after 20% TBSA full-thickness burn wound induction.…”

Section: Discussionsupporting

confidence: 71%

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

et al. 2020

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Severe burns may lead to intestinal inflammation and oxidative stress, resulting in intestinal barrier damage and gut dysfunction. Loganin, an iridoid glycoside compound, has been isolated from Cornus officinalis Sieb. et Zucc; however, its role in the treatment of burn injury is yet to be fully elucidated. Therefore, the present study examined the effect of loganin administration on burn-induced intestinal inflammation and oxidative stress after severe burns in male Sprague-Dawley rats. Histological injury was assessed by hematoxylin and eosin staining. Furthermore, cytokine expression in intestinal tissues was measured by ELISA and reverse transcription-quantitative PCR. Antioxidative activities were assessed by determining the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). Apoptosis was detected by flow cytometry. Apoptosis-related proteins, toll-like receptor 4 (TLR4) protein and NF-κB translocation were examined by western blotting. Immunohistochemical staining was used to observe TLR4 and NF-κB p65 expression in intestinal tissues. The present study suggested that loganin administration significantly reduced burn injury-induced intestinal histological changes, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β production and oxidative stress, evidenced by decreased ROS levels and MDA content (P<0.05). Furthermore, loganin increased SOD, CAT and GSH-Px levels and intestinal epithelial cell apoptosis. Loganin treatment also significantly inhibited activation of the TLR4/NF-κB signaling pathway in the intestine of severely burned rats (P<0.05). In conclusion, loganin reduced burns-induced intestinal inflammation and oxidative stress, potentially by regulating the TLR4/NF-κB signaling pathway.

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Section: Discussionsupporting

confidence: 71%

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

et al. 2020

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“…Burn injury has been shown to have a direct impact on intestinal function, including immune and barrier function ( Costantini et al, 2009 ). In addition, there was elevated level of serum IL-1β, intestinal edema and intestinal p38 MAPK activation in rats with severe burn injury ( Sun et al, 2017 ). These findings suggest that burn injury is closely associated with the intestinal damage, which may be accompanied by the gut microbial dysbiosis ( Huang et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Microbial community succession in the intestine of mice with deep partial-thickness burns

et al. 2023

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IntroductionBurn injury has been shown to lead to changes in the composition of the gut microbiome and cause other damage in patients. However, little is known about how the gut microbial community evolves in individuals who have recovered from burn injury.MethodsIn this study, we established a model of deep partial-thickness burn in mice and collected fecal samples at eight time points (pre-burn, 1, 3, 5, 7, 14, 21, and 28 days post-burn) for 16S rRNA amplification and high-throughput sequencing.ResultsThe results of the sequencing were analyzed using measures of alpha diversity, and beta diversity and taxonomy. We observed that the richness of the gut microbiome declined from day 7 post-burn and that the principal component and microbial community structure varied over time. On day 28 after the burn, the microbiome composition largely returned to the pre-burn level, although day 5 was a turning point for change. Some probiotics, such as the Lachnospiraceae_NK4A136_group, decreased in composition after the burn but were restored in the later recovery period. In contrast, Proteobacteria showed an opposite trend, which is known to include potential pathogenic bacteria.ConclusionThese findings demonstrate gut microbial dysbiosis after burn injury and provide new insights into the burn-related dysbiosis of the gut microbiome and strategies for improving the treatment of burn injury from the perspective of the microbiota.

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“…In accordance with our results, large area burns produce an obvious pathophysiologic inflammatory response and release a large number of proinflammatory mediators ( 21 ), including the influx of dendritic cells and macrophages, and M1 macrophages ( 22 , 23 ). In addition, the MAPK signaling pathway also plays an important role in the process of burn injury ( 24 , 25 ). These inflammatory mediators and signaling pathways can also be targets for burn treatment ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Molecular imbalance mechanism of skin and blood leucocytes in severe burn patients at different burn times

Liang¹,

Qiu²,

Wu³

et al. 2022

Ann Transl Med

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Background: Severe burns are a leading cause of injuries worldwide and are usually accompanied by considerable morbidity and mortality. The purpose of this study was to investigate the changes of gene expression in blood and skin at different times after severe burn.Methods: Firstly, the gene expression profiles of different burn time samples in GSE19743 and GSE8056 were analyzed. Secondly, the maladjusted gene network was identified by protein-protein interaction (PPI) network, and the genes in the network were enriched and analyzed. In addition, the key dysfunctional genes were identified by betweenness algorithm, and evaluated by survival analysis, Cox analysis, receiver operating characteristic (ROC) analysis. Finally, crosstalk analysis and enrichment analysis were carried out between the blood-and skin-specific differentially expressed genes (DEGs) at different burn times. Results:The results showed that there were common DEGs in the blood and skin at different burn times.Importantly, we screened out the key dysfunctional genes BIRC5, NCAM1, PCNA, TOP2A, and VEGFA, which were related to the course of burns. Enrichment analysis showed that these maladjusted genes were mainly involved in the immune inflammation-related signal pathway. Additionally, significant crosstalk was identified between blood-and skin-specific genes at different burn times, especially in the blood. The signal pathways involved in specific genes represent their own pathological characteristics.Conclusions: Both blood and skin tissues express common pathological changes and unique molecular mechanisms at different times after burn injury. The results of this study provide guidance for clinical personalized treatment.

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200 mM hypertonic saline resuscitation attenuates intestinal injury and inhibits p38 signaling in rats after severe burn trauma

Cited by 9 publications

References 54 publications

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

Microbial community succession in the intestine of mice with deep partial-thickness burns

Molecular imbalance mechanism of skin and blood leucocytes in severe burn patients at different burn times

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