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急性高压氧处理,与间歇性高压氧处理相反,由于氧化应激增加,会对健康 Sprague-Dawley 大鼠的血管舒张产生不利影响。

Acute Hyperbaric Oxygenation, Contrary to Intermittent Hyperbaric Oxygenation, Adversely Affects Vasorelaxation in Healthy Sprague-Dawley Rats due to Increased Oxidative Stress.

机构信息

Department of Physiology and Immunology, Faculty of Medicine, Josip Juraj Strossmayer University of Osijek, Cara Hadrijana 10E, 31 000 Osijek, Croatia.

出版信息

Oxid Med Cell Longev. 2018 Apr 29;2018:7406027. doi: 10.1155/2018/7406027. eCollection 2018.

DOI:10.1155/2018/7406027
PMID:29854092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5949176/
Abstract

The present study was aimed at assessing endothelium-dependent vasorelaxation, at measuring superoxide production in the aorta and femoral artery, and at determining antioxidative enzyme expression and activity in aortas of male Sprague-Dawley rats ( = 135), randomized to an A-HBO group exposed to a single hyperbaric oxygenation session (120' of 100% O at 2.0 bars), a 24H-HBO group (single session, examined 24 h after exposure), a 4D-HBO group (4 consecutive days of single sessions), and a CTRL group (untreated group). Vasorelaxation of aortic rings in response to acetylcholine (AChIR) and to reduced pO (HIR) was tested in vitro in the absence/presence of NOS inhibitor L-NAME and superoxide scavenger TEMPOL. eNOS, iNOS, antioxidative enzyme, and NADPH oxidase mRNA expression was assessed by qPCR. Serum oxidative stress markers and enzyme activity were assessed by spectrometry, and superoxide production was determined by DHE fluorescence. Impaired AChIR and HIR in the A-HBO group were restored by TEMPOL. L-NAME inhibited AChIR in all groups. Serum oxidative stress and superoxide production were increased in the A-HBO group compared to all other groups. The mRNA expression of iNOS was decreased in the A-HBO and 24H-HBO groups while SOD1 and 3 and NADPH oxidase were increased in the 4D-HBO group. The expression and activity of catalase and glutathione peroxidase were increased in the 4D-HBO group as well. AChIR was NO dependent. Acute HBO transiently impaired vasorelaxation due to increased oxidative stress. Vasorelaxation was restored and oxidative stress was normalized 24 h after the treatment.

摘要

本研究旨在评估内皮依赖性血管舒张功能,测量主动脉和股动脉中超氧化物的产生,并确定雄性 Sprague-Dawley 大鼠主动脉中抗氧化酶的表达和活性(n = 135),随机分为 A-HBO 组(暴露于单次高压氧治疗 120',100% O 2 ,2.0 个大气压)、24H-HBO 组(单次治疗,暴露后 24 小时检查)、4D-HBO 组(连续 4 天单次治疗)和对照组(未处理组)。在不存在/存在 NOS 抑制剂 L-NAME 和超氧化物清除剂 TEMPOL 的情况下,体外测试主动脉环对乙酰胆碱(AChIR)和还原 pO (HIR)的反应性。通过 qPCR 评估 eNOS、iNOS、抗氧化酶和 NADPH 氧化酶的 mRNA 表达。通过光谱法评估血清氧化应激标志物和酶活性,并通过 DHE 荧光测定超氧化物的产生。在 A-HBO 组中,TEMPOL 恢复了受损的 AChIR 和 HIR。L-NAME 抑制了所有组的 AChIR。与所有其他组相比,A-HBO 组的血清氧化应激和超氧化物产生增加。A-HBO 和 24H-HBO 组的 iNOS mRNA 表达降低,而 4D-HBO 组的 SOD1 和 3 以及 NADPH 氧化酶增加。4D-HBO 组的过氧化氢酶和谷胱甘肽过氧化物酶的表达和活性也增加。AChIR 是 NO 依赖性的。急性 HBO 短暂性地损害了血管舒张功能,这是由于氧化应激增加所致。治疗 24 小时后,血管舒张功能得到恢复,氧化应激得到正常化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/d5b8200b1568/OMCL2018-7406027.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/7d26fa66ac36/OMCL2018-7406027.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/1cf3f5947ec0/OMCL2018-7406027.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/e5334c5d16a3/OMCL2018-7406027.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/b9648a088707/OMCL2018-7406027.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/de6ea1558925/OMCL2018-7406027.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/b045fd27da8d/OMCL2018-7406027.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/23e3820fea24/OMCL2018-7406027.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/cae1b75ef1b5/OMCL2018-7406027.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/d5b8200b1568/OMCL2018-7406027.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/7d26fa66ac36/OMCL2018-7406027.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/1cf3f5947ec0/OMCL2018-7406027.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/e5334c5d16a3/OMCL2018-7406027.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/b9648a088707/OMCL2018-7406027.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/de6ea1558925/OMCL2018-7406027.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/b045fd27da8d/OMCL2018-7406027.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/23e3820fea24/OMCL2018-7406027.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/cae1b75ef1b5/OMCL2018-7406027.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f1b/5949176/d5b8200b1568/OMCL2018-7406027.009.jpg

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