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膳食硝酸盐可保护大鼠皮瓣免受缺血再灌注损伤:抗氧化作用的调节及炎症反应的减轻。

Dietary Nitrate Protects Against Skin Flap Ischemia-Reperfusion Injury in Rats Modulation of Antioxidative Action and Reduction of Inflammatory Responses.

作者信息

Cui Hao, Feng Yuanyong, Shu Chuanliang, Yuan Rongtao, Bu Lingxue, Jia Muyun, Pang Baoxing

机构信息

Department of Oral and Maxillofacial Surgery, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.

School of Stomatology of Qingdao University, Qingdao, China.

出版信息

Front Pharmacol. 2020 Jan 22;10:1605. doi: 10.3389/fphar.2019.01605. eCollection 2019.

DOI:10.3389/fphar.2019.01605
PMID:32038262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6987438/
Abstract

Dietary nitrate, found abundant in green vegetables, can be absorbed into the blood and be converted to nitric oxide (NO) in the body. Dietary nitrate has been proved to have many positive physiological functions in the body. Here, we evaluated the therapeutic effects of dietary nitrate on skin flap recovery following ischemia reperfusion (IR). Wistar rats were pretreated with nitrate from one week prior to ischemia to the end of reperfusion. It was found that oral administration of nitrate increased serum nitrate and nitrite levels, protected cells from apoptosis, and attenuated flap tissue edema. In the meantime, the oxidative stress marker malondialdehyde was reduced, while the activities of antioxidant enzymes were restored after nitrate treatment. Moreover, the macrophage and neutrophil infiltration in the flap was significantly attenuated by nitrate supplementation, as were the pro-inflammatory cytokines. In sum, we found that oral administration of nitrate can attenuate skin flap IR injury through the regulation of oxidative stress and inflammatory response.

摘要

膳食硝酸盐在绿色蔬菜中含量丰富,可被吸收进入血液并在体内转化为一氧化氮(NO)。膳食硝酸盐已被证明在体内具有许多积极的生理功能。在此,我们评估了膳食硝酸盐对缺血再灌注(IR)后皮瓣恢复的治疗效果。Wistar大鼠从缺血前一周至再灌注结束前用硝酸盐进行预处理。结果发现,口服硝酸盐可提高血清硝酸盐和亚硝酸盐水平,保护细胞免于凋亡,并减轻皮瓣组织水肿。同时,氧化应激标志物丙二醛减少,而硝酸盐处理后抗氧化酶的活性得以恢复。此外,补充硝酸盐可显著减轻皮瓣中巨噬细胞和中性粒细胞的浸润以及促炎细胞因子的水平。总之,我们发现口服硝酸盐可通过调节氧化应激和炎症反应减轻皮瓣IR损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bccf/6987438/9d55ff37b080/fphar-10-01605-g005.jpg
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