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含益生菌对创伤失血性休克大鼠肠黏膜的保护作用。

Protective effect of -containing probiotics on intestinal mucosa of rats experiencing traumatic hemorrhagic shock.

作者信息

Wang Lei, Liu Shu-Li, Xu Zhi-Peng, Song Qi, Li Lei, Qiu Zhao-Lei, Wang Zhen-Jie

机构信息

Department of Emergency, Anhui Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.

Department of Intensive Care Unit, The Second Affiliated Hospital of Shandong First Medical University, Tai'an, Shandong, 271000, China.

出版信息

Open Life Sci. 2021 Oct 11;16(1):1122-1129. doi: 10.1515/biol-2021-0112. eCollection 2021.

Abstract

This study was conducted to assess whether -containing probiotics could protect intestinal mucosa in rats during traumatic hemorrhagic shock and to determine its underlying mechanisms. Healthy male Sprague-Dawley rats (300 ± 20 g) were randomly divided into four groups. During the study, reverse transcription polymerase chain reaction, western blotting, and hematoxylin and eosin methods were used. There was a significant increase in the expression of toll-like receptor 4 (TLR4) in the rats that experienced traumatic hemorrhagic shock, along with increased mRNA of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. Pretreatment with -containing probiotics reduced TLR4 expression, decreased phosphorylation (Ser536) and acetylation (Lys310) of p65, and decreased TNF-α and IL-6 mRNA. The probiotics combined acetate Ringer's group showed a less severe pathological manifestation compared to the other experimental groups. -containing probiotics inhibited nuclear factor-kappa B signaling via the downregulation of TLR4, resulting in inflammatory homeostasis, which might be the mechanism whereby protects the intestinal mucosa from damage caused by the traumatic hemorrhagic shock.

摘要

本研究旨在评估含益生菌能否在创伤失血性休克期间保护大鼠肠黏膜,并确定其潜在机制。将健康雄性Sprague-Dawley大鼠(300±20 g)随机分为四组。在研究过程中,采用了逆转录聚合酶链反应、蛋白质印迹法和苏木精-伊红染色法。经历创伤失血性休克的大鼠中,Toll样受体4(TLR4)的表达显著增加,同时肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-6的mRNA也增加。含益生菌预处理可降低TLR4表达,减少p65的磷酸化(Ser536)和乙酰化(Lys310),并降低TNF-α和IL-6 mRNA。与其他实验组相比,益生菌联合醋酸林格液组的病理表现较轻。含益生菌通过下调TLR4抑制核因子-κB信号传导,从而实现炎症稳态,这可能是其保护肠黏膜免受创伤失血性休克损伤的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8773/8511963/b57c03c41336/j_biol-2021-0112-fig001.jpg

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