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Astaxanthin Protects OTA-Induced Lung Injury in Mice through the Nrf2/NF-κB Pathway

机译:虾青素通过Nrf2 /NF-κB途径保护OTA诱导的小鼠肺损伤

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摘要

The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-κB-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-κB) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-κB pathways.
机译:这项研究的目的是评估虾青素(ASTA)对小鼠肺中och曲毒素(OTA)引起的氧化损伤和炎症的潜在保护机制。我们将小鼠分为对照组(CG),OTA组(PG),虾青素组(AG)和OTA + ASTA组(JG)。氧化指数(丙二醛(MDA),总超氧化物歧化酶(T-SOD)和还原型谷胱甘肽(GSH))和炎性标志物(白介素1β(IL-1β),白介素6(IL-6)和肿瘤坏死因子α(在肺中测定TNF-α)),并计算肺重量与体重之比。通过TdT介导的dUTP缺口末端标记(TUNEL)分析检测到病理切片中的细胞凋亡。暴露于OTA后,在小鼠肺部检测到氧化损伤和炎症。此外,通过蛋白质印迹法检测到Nrf2-和NF-κB-通路相关蛋白。与OTA相比,ASTA显着提高了Nrf2,HO-1和MnSOD的表达,而其他蛋白质(Keap1,TLR4和NF-κB)的表达则明显降低。这些结果表明,ASTA通过调节Nrf2和NF-κB途径对OTA诱导的肺部氧化损伤和炎症具有保护作用。

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