Astaxanthin protects against early burn-wound progression in rats by attenuating oxidative stress-induced inflammation and mitochondria-related apoptosis.
Astaxanthin protects against early burn-wound progression in rats by attenuating oxidative stress-induced inflammation and mitochondria-related apoptosis.
复制标题
虾青素通过减轻氧化应激诱导的炎症和线粒体相关的细胞凋亡来防止大鼠早期烧伤伤口的进展
DOI：
10.1038/srep41440
复制
发表时间：
2017-01-27
影响因子：
4.6
通讯作者：
Han C
中科院分区：
文献类型：
--
作者：
Fang Q;Guo S;Zhou H;Han R;Wu P;Han C
深度烧伤后，烧伤创面进展可发生在烧伤初期或烧伤周围区域。停滞区因多种因素而恶化的风险较高，但也被认为是可以挽救的。从海洋生物中提取的虾青素（ATX）是一种天然化合物，具有很强的抗氧化作用，据报道可以减轻创伤性损伤引起的器官损伤。因此，我们研究了ATX对预防早期烧伤伤口进展的潜在作用。本研究建立了一种经典的“梳状”烧伤大鼠模型，用于组织学和生物学评估，其显示ATX，特别是较高剂量的ATX，减轻了瘀滞区的组织学恶化。此外，我们观察到ATX治疗后氧化应激和炎症介质释放的剂量依赖性改善。此外，ATX剂量依赖性衰减烧伤诱导的细胞凋亡的伤口区域，这种效果是伴随着Akt和Bad磷酸化和细胞色素C和半胱天冬酶的表达下调。此外，给予Ly 294002进一步验证了ATX的作用。总之，我们证明了ATX在大鼠深度烧伤模型中防止早期烧伤伤口进展。这种保护作用可能是通过减轻氧化应激诱导的炎症反应和细胞凋亡来介导的。
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.