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CD28 缺乏通过 PI3K/Akt 信号通路减弱小鼠原发性爆炸诱导的肾损伤。

CD28 deficiency attenuates primary blast-induced renal injury in mice via the PI3K/Akt signalling pathway.

机构信息

Emergency Medicine Department of General Hospital of Northern Theater Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, Shenyang, China.

Emergency Medicine Department of General Hospital of Northern Theater Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, Shenyang, China

出版信息

BMJ Mil Health. 2020 Nov;166(E):e66-e69. doi: 10.1136/jramc-2019-001181. Epub 2019 May 24.

DOI:10.1136/jramc-2019-001181
PMID:31129646
Abstract

INTRODUCTION

Primary blast affects the kidneys due to direct shock wave damage and the production of proinflammatory cytokines without effective treatment. CD28 has been reported to be involved in regulating T cell activation and secretion of inflammatory cytokines. The aim of this study was to investigate the influence of primary blast on the kidney and the effect of CD28 in mice.

METHODS

A mouse model of primary blast-induced kidney injury was established using a custom-made explosive device. The severity of kidney injury was investigated by H&E staining. ELISA was applied to study serum inflammation factors' expression. Western blot assays were used to analyse the primary blast-induced inflammatory factors' expression in the kidney. Immunofluorescence analysis was used to examine the PI3K/Akt signalling pathway.

RESULTS

Histological examination demonstrated that compared with the primary blast group, CD28 deficiency caused a significant decrease in the severity of the primary blast-induced renal injury. Moreover, ELISA and western blotting revealed that CD28 deficiency significantly reduced the levels of interleukin (IL)-1β, IL-4 and IL-6, and increased the IL-10 level (p<0.05). Finally, immunofluorescence analysis indicated that PI3K/Akt expression also changed.

CONCLUSIONS

CD28 deficiency had protective effects on primary blast-induced kidney injury via the PI3K/Akt signalling pathway. These findings improve the knowledge on primary blast injury and provide theoretical basis for primary blast injury treatment.

摘要

简介

原发性爆炸会直接通过冲击波损伤和产生促炎细胞因子而影响肾脏,若不进行有效治疗,后果将十分严重。CD28 已被报道参与调节 T 细胞激活和炎症细胞因子的分泌。本研究旨在探讨原发性爆炸对肾脏的影响,以及 CD28 在其中的作用。

方法

使用定制的爆炸装置建立了原发性爆炸诱导的肾损伤小鼠模型。通过 H&E 染色研究肾损伤的严重程度。ELISA 用于研究血清炎症因子的表达。Western blot 分析用于分析原发性爆炸诱导的肾脏中炎症因子的表达。免疫荧光分析用于检测 PI3K/Akt 信号通路。

结果

组织学检查表明,与原发性爆炸组相比,CD28 缺乏导致原发性爆炸诱导的肾损伤严重程度显著降低。此外,ELISA 和 Western blot 揭示,CD28 缺乏显著降低了白细胞介素(IL)-1β、IL-4 和 IL-6 的水平,并增加了 IL-10 的水平(p<0.05)。最后,免疫荧光分析表明 PI3K/Akt 表达也发生了变化。

结论

CD28 缺乏通过 PI3K/Akt 信号通路对原发性爆炸诱导的肾损伤具有保护作用。这些发现增进了对原发性爆炸损伤的认识,并为原发性爆炸损伤的治疗提供了理论依据。

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