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卡马西平对失血性休克再灌注大鼠急性肺损伤的保护作用。

The protective effect of carbamazepine on acute lung injury induced by hemorrhagic shock and resuscitation in rats.

机构信息

Department of Anesthesiology and Resuscitology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.

Department of Anesthesiology and Resuscitology, Okayama University Medical School, Okayama, Japan.

出版信息

PLoS One. 2024 Oct 23;19(10):e0309622. doi: 10.1371/journal.pone.0309622. eCollection 2024.

DOI:10.1371/journal.pone.0309622
PMID:39441839
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11498730/
Abstract

Hemorrhagic shock and resuscitation (HSR) enhances the risk of acute lung injury (ALI). This study investigated the protective effect of carbamazepine (CBZ) on HSR-induced ALI in rats. Male Sprague-Dawley rats were allocated into five distinct groups through randomization: control (SHAM), saline + HSR (HSR), CBZ + HSR (CBZ/HSR), dimethyl sulfoxide (DMSO) + HSR (DMSO/HSR), and CBZ + chloroquine (CQ) + HSR (CBZ/CQ/HSR). Subsequently, HSR models were established. To detect tissue damage, we measured lung histological changes, lung injury scores, and wet/dry weight ratios. We measured neutrophil counts as well as assessed the expression of inflammatory factors using RT-PCR to determine the inflammatory response. We detected autophagy-related proteins LC3II/LC3I, P62, Beclin-1, and Atg12-Atg5 using western blotting. Pretreatment with CBZ improved histopathological changes in the lungs and reduced lung injury scores. The CBZ pretreatment group exhibited significantly reduced lung wet/dry weight ratio, neutrophil aggregation and number, and inflammation factor (TNF-α and iNOS) expression. CBZ changed the expression levels of autophagy-related proteins (LC3II/LC3I, beclin-1, Atg12-Atg5, and P62), suggesting autophagy activation. However, after injecting CQ, an autophagy inhibitor, the beneficial effects of CBZ were reversed. Taken together, CBZ pretreatment improved HSR-induced ALI by suppressing inflammation, at least in part, through activating autophagy. Thus, our study offers a novel perspective for treating HSR-induced ALI.

摘要

出血性休克和复苏 (HSR) 增加了急性肺损伤 (ALI) 的风险。本研究探讨了卡马西平 (CBZ) 对大鼠 HSR 诱导的 ALI 的保护作用。雄性 Sprague-Dawley 大鼠通过随机化分配到五个不同的组：对照组 (SHAM)、生理盐水+HSR (HSR)、CBZ+HSR (CBZ/HSR)、二甲基亚砜 (DMSO)+HSR (DMSO/HSR) 和 CBZ+氯喹 (CQ)+HSR (CBZ/CQ/HSR)。随后，建立了 HSR 模型。为了检测组织损伤，我们测量了肺组织学变化、肺损伤评分和湿/干重比。我们测量了中性粒细胞计数，并通过 RT-PCR 评估了炎症因子的表达，以确定炎症反应。我们使用 Western blot 检测自噬相关蛋白 LC3II/LC3I、P62、Beclin-1 和 Atg12-Atg5 的表达。CBZ 预处理改善了肺组织的组织学变化，降低了肺损伤评分。CBZ 预处理组的肺湿/干重比、中性粒细胞聚集和数量以及炎症因子 (TNF-α 和 iNOS) 表达显著降低。CBZ 改变了自噬相关蛋白 (LC3II/LC3I、beclin-1、Atg12-Atg5 和 P62) 的表达水平，提示自噬激活。然而，在注射自噬抑制剂 CQ 后，CBZ 的有益作用被逆转。总之，CBZ 预处理通过抑制炎症至少部分通过激活自噬改善了 HSR 诱导的 ALI。因此，我们的研究为治疗 HSR 诱导的 ALI 提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/2d6b35a9a4b1/pone.0309622.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/b86624bc8b10/pone.0309622.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/2b6428e5a62f/pone.0309622.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/2d6b35a9a4b1/pone.0309622.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/b86624bc8b10/pone.0309622.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/199e9417ee87/pone.0309622.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/ff1d64eba739/pone.0309622.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/2b6428e5a62f/pone.0309622.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77df/11498730/2d6b35a9a4b1/pone.0309622.g005.jpg

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