脂质过氧化
脑损伤
大脑皮质
氧化损伤
氧化应激
内分泌学
内科学
血压
谷胱甘肽
医学
病态的
皮质(解剖学)
GPX4
脑组织
化学
过氧化氢酶
生物化学
生物
谷胱甘肽过氧化物酶
神经科学
酶
作者
Jian Yang,Min Wang,Wang Shu,Guiping Li,Ying Gao
标识
DOI:10.1080/10641963.2020.1783545
摘要
Objective This study aimed to explore the mechanism of hypertensive brain damage from ferroptosis pathway.Methods Ten 22-week-old SHR rats were labeled as hypertension group(HBP), while ten WKY rats of comparable age, weight were used as normal blood pressure group(NBP). After 2 weeks of feeding, hypertensive brain damage was observed by comparing the pathological changes of brain tissue in SHR rats and WKY rats. Furthermore, the expression of GPX4 in the cerebral cortex was detected by immunofluorescence. The content of GSH was determined by spectrophotometer. The content of iron was detected by ferrous chromite colorimetry. And the content of MDA was determined by spectrophotometer. Compare the difference to investigate the role of ferroptosis mechanism in hypertensive brain damage.Results Brain damage occurred in 24-week-old SHR rats compared with WKY rats. In the HBP, the GPX4 and GSH were significantly lower than those in the NBP, and the total iron content and MDA were significantly increased.Conclusion Thses findings suggest ferroptosis is closely related to hypertensive brain damage. Elevated blood pressure leads to iron overload in the brain. Excessive iron increases oxidative stress and lipid peroxidation in the brain, and eventually causes brain damage.
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