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阿普米拉斯通过调节氧化应激和炎症对脂多糖诱导的急性肺损伤的保护作用。

Protective effect of Apremilast against LPS-induced acute lung injury via modulation of oxidative stress and inflammation.

作者信息

Al-Harbi Naif O, Imam Faisal, Al-Harbi Mohammad Matar, Aljeryan Khaldoon, Al-Shabanah Othman A, Alhosaini Khaled A, Alqahtani Lamya Saif, Afzal Muhammad, Khalid Anwer M D, Aldossari Abdullah A, Alanazi Mohammed M, Alsanea Sary, Assiri Mohammed A

机构信息

Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia.

Department of Pathology, College of Medicine, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia.

出版信息

Saudi J Biol Sci. 2022 May;29(5):3414-3424. doi: 10.1016/j.sjbs.2022.02.023. Epub 2022 Feb 23.

DOI:10.1016/j.sjbs.2022.02.023
PMID:35844406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9280219/
Abstract

Lung injuries are attributed due to exposure to Drugs or chemicals. One of the important challenging situations for the clinicians is to manage treatments of different diseases with acute lung injury (ALI). The objective of this study was to investigate the possible protective mechanisms and action of a novel Phosphodiesterase-4 inhibitor "Apremilast" (AP) in lipopolysaccharide (LPS)-induced lung injury. Blood sample from each animals were collected in a vacuum blood collection tube. The rat lungs were isolated for oxidative stress assessment, western blot analysis and their mRNA expressions using RT-PCR. Exposure of LPS in rats causes significant increase in oxidative stress, activates the pro-inflammatory cytokines release like tissue necrotic factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), modulated gene expression, protein expression and histopathological changes which were reversed by administration of AP. Finding of the research enlighten the protective role of AP against LPS-induced ALI.

摘要

肺损伤归因于接触药物或化学物质。对于临床医生来说,重要的挑战之一是管理患有急性肺损伤(ALI)的不同疾病的治疗。本研究的目的是研究新型磷酸二酯酶-4抑制剂“阿普司他”(AP)在脂多糖(LPS)诱导的肺损伤中的可能保护机制和作用。将每只动物的血样收集到真空采血管中。分离大鼠肺用于氧化应激评估、蛋白质印迹分析及其使用逆转录聚合酶链反应(RT-PCR)的mRNA表达。大鼠暴露于LPS会导致氧化应激显著增加,激活促炎细胞因子如组织坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的释放,调节基因表达、蛋白质表达和组织病理学变化,而AP给药可逆转这些变化。该研究结果揭示了AP对LPS诱导的ALI的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/3738da098e5f/gr13.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/3738da098e5f/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/487a2ddb9933/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/b32b93c39677/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/bf753a05887b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/7c67e4e447ed/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/90946cde4ea1/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/01a1ea2d9847/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/a17d10abbec2/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/81ea97108f39/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/c7bd71eedfac/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/fd513f177845/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/5a17fb458070/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/7f90bd2d0d9c/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92fd/9280219/3738da098e5f/gr13.jpg

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