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从蓝绿藻中提取的藻蓝蛋白对脂多糖诱导的急性肺损伤大鼠模型的治疗作用。

Therapeutic effect of C-phycocyanin extracted from blue green algae in a rat model of acute lung injury induced by lipopolysaccharide.

机构信息

Department of Intensive Care, Chi Mei Medical Center Liou Ying Campus, Tainan, Taiwan.

出版信息

Evid Based Complement Alternat Med. 2013;2013:916590. doi: 10.1155/2013/916590. Epub 2013 Mar 20.

DOI:10.1155/2013/916590
PMID:23573157
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3615630/
Abstract

C-Phycocyanin (CPC), extracted from blue green algae, is a dietary nutritional supplement due to its several beneficial pharmacological effects. This study was conducted to evaluate whether CPC protects against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in rats. Rats were challenged with LPS (5 mg/kg body weight) intratracheally to induce ALI. After 3 h LPS instillation, rats were administrated with CPC (50 mg/kg body weight, i.p.) for another 3 h. Our results showed that posttreatment with CPC significantly inhibited LPS-induced elevation of protein concentration, nitrite/nitrate level, release of proinflammatory cytokines, the number of total polymorphonuclear cells in bronchoalveolar lavage fluid, and lung edema evidenced by decrease of lung wet/dry weight ratio accompanied by a remarkable improvement of lung histopathological alterations. Furthermore, CPC significantly attenuated LPS-induced myeloperoxidase activity, O2 (-) formation, expression of inducible nitric oxide synthase, and cyclooxygenase-2 as well as nuclear factor-kappa B (NF- κ B) activation in lungs. Additionally, CPC significantly downregulated proapoptotic proteins such as caspase-3 and Bax, but upregulated antiapoptotic proteins such as Bcl-2 and Bcl-XL in lungs exposed to LPS. These findings indicate that CPC could be potentially useful for treatment of LPS-related ALI by inhibiting inflammatory responses and apoptosis in lung tissues.

摘要

藻蓝蛋白(CPC)从蓝绿藻中提取,具有多种有益的药理作用,因此被用作膳食营养补充剂。本研究旨在评估 CPC 是否对脂多糖(LPS)诱导的大鼠急性肺损伤(ALI)具有保护作用。通过气管内滴注 LPS(5mg/kg 体重)建立大鼠 ALI 模型。LPS 滴注 3 小时后,腹腔内给予 CPC(50mg/kg 体重)处理 3 小时。结果表明,CPC 后处理显著抑制了 LPS 诱导的蛋白浓度、亚硝酸盐/硝酸盐水平、促炎细胞因子释放、支气管肺泡灌洗液中总多形核细胞数量以及肺湿/干重比的增加,从而减轻肺水肿,肺组织病理学改变也得到显著改善。此外,CPC 还显著抑制了 LPS 诱导的髓过氧化物酶活性、O2(-)形成、诱导型一氧化氮合酶和环氧化酶-2的表达以及核因子-κB(NF- κ B)在肺组织中的激活。同时,CPC 还显著下调了 LPS 诱导的肺组织中促凋亡蛋白如 caspase-3 和 Bax 的表达,上调了抗凋亡蛋白如 Bcl-2 和 Bcl-XL 的表达。这些结果表明,CPC 可能通过抑制肺组织中的炎症反应和细胞凋亡,对 LPS 相关的 ALI 具有潜在的治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/17964cd01c3b/ECAM2013-916590.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/91b6ba0bb9b1/ECAM2013-916590.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/f2f33fe9d97d/ECAM2013-916590.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/677c8c2c1d41/ECAM2013-916590.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/b166fd118ec8/ECAM2013-916590.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/6c69818494e7/ECAM2013-916590.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/17964cd01c3b/ECAM2013-916590.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/91b6ba0bb9b1/ECAM2013-916590.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/f2f33fe9d97d/ECAM2013-916590.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/677c8c2c1d41/ECAM2013-916590.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/b166fd118ec8/ECAM2013-916590.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/6c69818494e7/ECAM2013-916590.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2dc/3615630/17964cd01c3b/ECAM2013-916590.006.jpg

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