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白藜芦醇通过激活 Sirt1 缓解新生大鼠高氧诱导的脑损伤。

Resveratrol Relieves Hyperoxia-Induced Brain Injury in Neonatal Rats by Activating Sirt1.

机构信息

Department of Newborn Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

Department of Burns and Plastic Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

出版信息

Am J Perinatol. 2021 Aug;38(S 01):e351-e358. doi: 10.1055/s-0040-1710352. Epub 2020 May 1.

DOI:10.1055/s-0040-1710352
PMID:32357375
Abstract

OBJECTIVE

Neonatal rats with hyperoxia-induced brain injury were treated with resveratrol to investigate its protective effects through analyzing changes in reactive oxygen species (ROS), Sirt1, p53, and acetylated p53 levels.

STUDY DESIGN

Neonatal rats were randomly divided into hyperoxia and resveratrol intervened groups. Rats in both groups were placed in a hyperoxia chamber for 7 days to induce hyperoxia-induced brain injury. The rats in the resveratrol intervened group were administered resveratrol 60 μg/g body weight daily, whereas those in the hyperoxia group were administered a dimethyl sulfoxide-based solvent. Brain tissues were collected, and hematoxylin and eosin (H&E) and TUNEL staining, ROS measurements, real time-polymerase chain reaction, and western blotting were performed.

RESULTS

H&E and TUNEL staining revealed increased cell damage and apoptosis in brain tissue from hyperoxia-exposed animals compared with the findings in animals in the resveratrol intervened group. Real time-polymerase chain reaction and western blotting identified increases in Sirt1 expression and decreases in p53 expression in the resveratrol intervened group. In addition, acetylated p53 protein expression was lower in the intervened group than in the hyperoxia group.

CONCLUSION

Resveratrol alleviated brain apoptosis induced by hyperoxia in neonatal rats by upregulating Sirt1-mediated pathways, suggesting its potentially beneficial role in the treatment of brain injury induced by hyperoxia.

摘要

目的

通过分析活性氧(ROS)、Sirt1、p53 和乙酰化 p53 水平的变化,研究白藜芦醇对高氧诱导脑损伤新生大鼠的保护作用。

研究设计

将新生大鼠随机分为高氧组和白藜芦醇干预组。两组大鼠均置于高氧室中 7 天以诱导高氧诱导脑损伤。白藜芦醇干预组大鼠每日给予白藜芦醇 60μg/g 体重,高氧组大鼠给予二甲基亚砜溶剂。收集脑组织,进行苏木精和伊红(H&E)及 TUNEL 染色、ROS 测定、实时聚合酶链反应和 Western blot 分析。

结果

与白藜芦醇干预组相比,高氧暴露动物的脑组织 H&E 和 TUNEL 染色显示细胞损伤和凋亡增加。实时聚合酶链反应和 Western blot 鉴定出白藜芦醇干预组 Sirt1 表达增加,p53 表达减少。此外,干预组的乙酰化 p53 蛋白表达低于高氧组。

结论

白藜芦醇通过上调 Sirt1 介导的途径缓解新生大鼠高氧诱导的脑凋亡,提示其在治疗高氧诱导脑损伤方面具有潜在的有益作用。

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