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虾青素通过减轻氧化应激诱导的炎症和线粒体相关凋亡来防止大鼠早期烧伤创面进展。

Astaxanthin protects against early burn-wound progression in rats by attenuating oxidative stress-induced inflammation and mitochondria-related apoptosis.

机构信息

Department of Burns, Second Affiliated Hospital, Zhejiang University, College of Medicine, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China.

Department of Plastic Surgery, Binjiang Branch, Second Affiliated Hospital, Zhejiang University, College of Medicine, 1511 Jianghong Road, Hangzhou 310000, Zhejiang, China.

出版信息

Sci Rep. 2017 Jan 27;7:41440. doi: 10.1038/srep41440.

DOI:10.1038/srep41440
PMID:28128352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5269753/
Abstract

Burn-wound progression can occur in the initial or peri-burn area after a deep burn injury. The stasis zone has a higher risk of deterioration mediated by multiple factors but is also considered salvageable. Astaxanthin (ATX), which is extracted from some marine organisms, is a natural compound with a strong antioxidant effect that has been reported to attenuate organ injuries caused by traumatic injuries. Hence, we investigated the potential effects of ATX on preventing early burn-wound progression. A classic "comb" burn rat model was established in this study for histological and biological assessments, which revealed that ATX, particularly higher doses, alleviated histological deterioration in the stasis zone. Additionally, we observed dose-dependent improvements in oxidative stress and the release of inflammatory mediators after ATX treatment. Furthermore, ATX dose-dependently attenuated burn-induced apoptosis in the wound areas, and this effect was accompanied by increases in Akt and Bad phosphorylation and a downregulation of cytochrome C and caspase expression. In addition, the administration of Ly 294002 further verified the effect of ATX. In summary, we demonstrated that ATX protected against early burn-wound progression in a rat deep-burn model. This protection might be mediated by the attenuation of oxidative stress-induced inflammation and mitochondria-related apoptosis.

摘要

烧伤创面进展可发生于深度烧伤后的初始或烧伤周边区。淤血区恶化的风险更高,受多种因素影响,但也被认为是可挽救的。虾青素(ATX)是从某些海洋生物中提取的天然化合物,具有很强的抗氧化作用,据报道可减轻创伤引起的器官损伤。因此,我们研究了 ATX 预防早期烧伤创面进展的潜在作用。本研究建立了经典的“梳子”烧伤大鼠模型,用于组织学和生物学评估,结果表明 ATX,特别是高剂量,可减轻淤血区的组织恶化。此外,我们观察到 ATX 治疗后氧化应激和炎症介质释放呈剂量依赖性改善。此外,ATX 剂量依赖性地减轻了创面处烧伤诱导的细胞凋亡,这种作用伴随着 Akt 和 Bad 磷酸化的增加以及细胞色素 C 和 caspase 表达的下调。此外,给予 Ly 294002 进一步验证了 ATX 的作用。总之,我们证明了 ATX 可预防大鼠深度烧伤模型中的早期烧伤创面进展。这种保护作用可能是通过减轻氧化应激诱导的炎症和线粒体相关凋亡介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/29b4a2949065/srep41440-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/ee45bf5a650d/srep41440-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/7d29d5498184/srep41440-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/0bd76ea3c957/srep41440-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/29b4a2949065/srep41440-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/ee45bf5a650d/srep41440-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/6fdefe6f4c53/srep41440-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/de834349e51e/srep41440-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/25bf90b093ff/srep41440-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/c2443ec05a03/srep41440-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/7d29d5498184/srep41440-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/0bd76ea3c957/srep41440-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40ca/5269753/29b4a2949065/srep41440-f8.jpg

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