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银杏叶提取物(EGb 761)对急性缺氧后老龄大鼠脑不同区域氧化应激参数的影响。

The effect of Ginkgo biloba extract (EGb 761) on parameters of oxidative stress in different regions of aging rat brains after acute hypoxia.

机构信息

Institute of Laboratory Medicine, Clinical Chemistry, and Molecular Diagnostics, Department of Medicine, University of Leipzig, Germany.

出版信息

Aging Clin Exp Res. 2011 Aug;23(4):255-63. doi: 10.1007/BF03337752. Epub 2010 Aug 27.

Abstract

BACKGROUND AND AIMS

Neurodegenerative processes of aging seem to be associated with oxidative stress by reactive oxygen species (ROS). This study investigates the influence of age and of acute respiratoric hypoxia on parameters of oxidative stress in different brain regions of Wistar rats and the protective effects of Ginkgo extract (EGb 761) as a radical scavenger.

METHODS

Biopsies of frontal and temporal cortices, the cerebellum, and the brainstem of young and old rats (each group n=6-8: normoxic - hypoxic; unprotected - EGb-protected) were analyzed for malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione (GSH) content, and creatine kinase (CK) activity. Experimental hypoxia: downregulation of oxygen partial pressure to 5 vol. % for 20 minutes. EGb administration: daily 100 mg/kg of body weight in drinking water for 3 months.

RESULTS

Effects of age: While most oxidative stress parameters in the temporal cortex, the cerebellum, and the brainstem are increased, this is not the case in the frontal cortex; after additional hypoxia SOD and GSH are diminished in the temporal cortex and the brainstem of old rats. EGb treatment causes contradictory alterations in young, old, and hypoxic brain regions. Minor effects are seen in old hypoxic brains, while there are some protective effects in old normoxic brainstems and cerebellums.

CONCLUSIONS

The old brain appears to adapt appropriately to chronic oxidative stress and to the specific conditions of shortterm hypoxia. EGb's protective effect is especially notable in the brainstem and the cerebellum.

摘要

背景与目的

衰老过程中的神经退行性变化似乎与活性氧(ROS)引起的氧化应激有关。本研究旨在探讨年龄和急性呼吸性缺氧对 Wistar 大鼠不同脑区氧化应激参数的影响,以及银杏提取物(EGb 761)作为自由基清除剂的保护作用。

方法

对年轻和年老大鼠(每组 n=6-8:常氧-缺氧;未保护-EGb 保护)的额皮质和颞皮质、小脑和脑干进行活检,分析丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)含量和肌酸激酶(CK)活性。实验性缺氧:下调氧分压至 5 体积%20 分钟。EGb 给药:每天饮用 100mg/kg 体重的水,持续 3 个月。

结果

年龄的影响:虽然颞皮质、小脑和脑干中的大多数氧化应激参数增加,但额皮质并非如此;在老年大鼠中,另外的缺氧会导致颞皮质和脑干中的 SOD 和 GSH 减少。EGb 处理在年轻、年老和缺氧脑区引起相反的改变。老年缺氧脑区的影响较小,而老年正常脑桥和小脑则有一定的保护作用。

结论

老年大脑似乎能很好地适应慢性氧化应激和短期缺氧的特殊条件。EGb 的保护作用在脑干和小脑尤为明显。

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