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肾上腺髓质素减轻大鼠高氧肺损伤。

Attenuation of hyperoxia-induced lung injury in rats by adrenomedullin.

机构信息

Department of Thoracic Surgery, Subei People's Hospital of Jiangsu province, Jiangsu, 225001, People's Republic of China.

出版信息

Inflammation. 2012 Feb;35(1):150-7. doi: 10.1007/s10753-011-9300-1.

DOI:10.1007/s10753-011-9300-1
PMID:21302135
Abstract

Oxidative stress and inflammation are involved in the pathogenesis of acute lung injury (ALI). Adrenomedullin (AM) is an endogenous peptide with anti-inflammatory and antioxidant properties. This study investigated that whether AM treatment may ameliorate hyperoxia-induced ALI in rats via inhibition of oxidative stress and inflammation. Rats were randomized to receive continuous intravenous infusion of AM or saline through a microosmotic pump, and then ALI was induced by exposing the animals in sealed cages >95% oxygen for 72 h. Exposure to hyperoxia caused lung injury as increased infiltration of inflammatory cells and disruption of lung architecture. AM administration markedly improved these changes. Additionally, AM administration significantly increased glutathione peroxidase and superoxide dismutase activities. Meanwhile, hyperoxia-induced increase of lipid hydroperoxide level was markedly reduced by AM treatment. Moreover, nuclear factor-kappa B-DNA-binding activity, and production of the inflammatory mediators interleukin-6, keratinocyte-derived chemokine, and matrix metalloproteinase 9, were significantly inhibited by AM treatment. AM ameliorates hyperoxia-induced ALI in rats by suppression of oxidative stress and inflammation.

摘要

氧化应激和炎症参与急性肺损伤 (ALI) 的发病机制。肾上腺髓质素 (AM) 是一种具有抗炎和抗氧化特性的内源性肽。本研究探讨了 AM 治疗是否可以通过抑制氧化应激和炎症来改善高氧诱导的大鼠 ALI。大鼠通过微渗透泵接受持续静脉输注 AM 或生理盐水,并在密封笼中暴露于 >95%氧气中 72 小时以诱导 ALI。暴露于高氧会导致肺损伤,表现为炎症细胞浸润增加和肺结构破坏。AM 给药显著改善了这些变化。此外,AM 给药显著增加了谷胱甘肽过氧化物酶和超氧化物歧化酶的活性。同时,AM 处理明显降低了高氧诱导的脂质过氧化物水平升高。此外,AM 处理还显著抑制了核因子-κB-DNA 结合活性以及炎症介质白细胞介素-6、角质细胞衍生趋化因子和基质金属蛋白酶 9 的产生。AM 通过抑制氧化应激和炎症改善高氧诱导的大鼠 ALI。

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