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缺血后处理减轻脂多糖诱导的大鼠急性肺损伤。

Ischemic Postconditioning Mitigates Lipopolysaccharide-induced Acute Lung Injury in Rats.

机构信息

Department of Chest Disease, Trakya University Faculty of Medicine, Edirne, Turkey;

Department of Physiology, Trakya University Faculty of Medicine, Edirne, Turkey.

出版信息

In Vivo. 2024 Nov-Dec;38(6):2705-2711. doi: 10.21873/invivo.13748.

DOI:10.21873/invivo.13748
PMID:39477422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11535931/
Abstract

BACKGROUND/AIM: Acute lung injury (ALI) is a syndrome characterized by the disruption of alveolar endothelial and epithelial barriers, neutrophilic infiltration in pulmonary regions, and non-cardiogenic edema, associated with high mortality and morbidity. Despite intensive research efforts, there is currently no approved specific treatment for the condition. The aim of this study was to investigate the potential beneficial effect of ischemic post-conditioning in lipopolysaccharide (LPS)-induced lung injury and its possible association with inflammatory and apoptotic processes.

MATERIALS AND METHODS

Lung injury was induced in rats by a single intraperitoneal administration of 10 mg/kg LPS. Under anesthesia, latex tourniquets were wrapped around both hind limbs of the animals in a region close to the body to achieve complete ischemia. The ischemic conditioning procedure consisted of four cycles of 10 min of ischemia followed by 10 min of reperfusion. Inflammation, and apoptosis levels were measured using ELISA. Hematoxylin and eosin staining was used for histopathological evaluation, while TUNEL staining was employed for apoptotic cell counting. One-way analysis of variance (ANOVA) with post hoc Tukey test was used for comparisons between groups.

RESULTS

Intraperitoneal LPS administration induced neutrophil infiltration and apoptotic cell death in lung tissue. These effects were prevented by remote ischemic postconditioning (RIPostC) application. Additionally, the beneficial effects of ischemic conditioning can be transferred via serum.

CONCLUSION

RIPostC can ameliorate LPS-induced ALI. The mechanism of the protective effects of RIPostC may lie in the suppression of apoptosis and neutrophil infiltration.

摘要

背景/目的:急性肺损伤(ALI)是一种以肺泡内皮和上皮屏障破坏、肺组织中性粒细胞浸润和非心源性水肿为特征的综合征,其死亡率和发病率都很高。尽管进行了大量的研究,但目前尚无针对该疾病的特效治疗方法。本研究旨在探讨缺血后处理(ischemic post-conditioning,IPC)对脂多糖(lipopolysaccharide,LPS)诱导的肺损伤的潜在有益作用及其与炎症和凋亡过程的可能联系。

材料和方法

通过单次腹腔内给予 10 mg/kg LPS 诱导大鼠肺损伤。在麻醉下,乳胶止血带缠绕在动物靠近身体的两条后肢上,以实现完全缺血。IPC 程序包括四个周期的 10 分钟缺血,随后进行 10 分钟再灌注。使用 ELISA 测量炎症和凋亡水平。苏木精和伊红染色用于组织病理学评估,TUNEL 染色用于计数凋亡细胞。采用单因素方差分析(one-way analysis of variance,ANOVA)和事后 Tukey 检验进行组间比较。

结果

腹腔内 LPS 给药诱导了肺组织中的中性粒细胞浸润和凋亡细胞死亡。IPC 应用可预防这些效应。此外,IPC 的有益作用可通过血清传递。

结论

IPC 可以改善 LPS 诱导的 ALI。IPC 保护作用的机制可能在于抑制凋亡和中性粒细胞浸润。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/93570b42f1aa/in_vivo-38-2710-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/c6018a580349/in_vivo-38-2707-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/c18b6d9064e7/in_vivo-38-2708-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/0affa6e79ca7/in_vivo-38-2709-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/93570b42f1aa/in_vivo-38-2710-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/c6018a580349/in_vivo-38-2707-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/c18b6d9064e7/in_vivo-38-2708-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/0affa6e79ca7/in_vivo-38-2709-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca50/11535931/93570b42f1aa/in_vivo-38-2710-g0001.jpg

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