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20-羟基蜕皮甾酮改善链脲佐菌素诱导的 1 型糖尿病大鼠记忆缺陷的作用。

Effects of 20-hydroxyecdysone on improving memory deficits in streptozotocin-induced type 1 diabetes mellitus in rat.

机构信息

Basal Medicine College of Nanyang Medical University, Nanyang 473041, Henan Province, China.

Basal Medicine College of Nanyang Medical University, Nanyang 473041, Henan Province, China.

出版信息

Eur J Pharmacol. 2014 Oct 5;740:45-52. doi: 10.1016/j.ejphar.2014.06.026. Epub 2014 Jul 2.

Abstract

We investigate the effects of 20-hydroxyecdysone (20E) on improving memory deficits in the current study by using an animal model of type 1 diabetes mellitus in rats. Animals in control group went on a normal diet. Rats that developed diabetes were divided into 4 groups, including STZ-induced diabetic group which was treated with saline and three 20E groups received different 20E concentrations for 12 weeks. Spatial memory performance was measured in rats by the Morris water maze. The level of nuclear factor-кB (NF-кB) in the brain was determined by real-time quantitative PCR. The mRNA levels and enzyme activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GR) were analyzed by real-time quantitative PCR and spectrophotometry. The concentrations of brain-derived neurotrophic factor (BDNF) in the brain were detected by ELISA. Compared with the control group, rats in the STZ-induced diabetic group that developed type 1 diabetes exhibited significant memory loss. In addition to the hippocampus CA1 area that displayed severe damage, significantly higher expression levels of NF-кB were observed in these rats. Furthermore, the expression levels of SOD, catalase, GSH-Px GR and BDNF were significantly decreased in rats with diabetes. By contrast, the treatment with 20E, especially at higher concentrations, reversed the above-mentioned conditions caused by diabetes. The results suggest that the 20E has a protective role in counteracting memory deficits in rats with diabetes of rat, possibly through enhancing the antioxidative ability in the brain.

摘要

我们通过建立大鼠 1 型糖尿病动物模型,研究了 20-羟基蜕皮甾酮(20E)改善记忆缺陷的作用。对照组动物给予正常饮食。糖尿病大鼠分为 4 组,包括用生理盐水治疗的 STZ 诱导的糖尿病组和接受不同浓度 20E 治疗 12 周的 3 个 20E 组。通过 Morris 水迷宫检测大鼠的空间记忆能力。实时定量 PCR 测定脑核因子-кB(NF-кB)水平。实时定量 PCR 和分光光度法分析超氧化物歧化酶(SOD)、过氧化氢酶、谷胱甘肽过氧化物酶(GSH-Px)和谷胱甘肽还原酶(GR)的 mRNA 水平和酶活性。脑源性神经营养因子(BDNF)的浓度通过 ELISA 检测。与对照组相比,发生 1 型糖尿病的 STZ 诱导的糖尿病大鼠表现出明显的记忆丧失。除了海马 CA1 区严重损伤外,这些大鼠的 NF-кB 表达水平也显著升高。此外,糖尿病大鼠 SOD、过氧化氢酶、GSH-Px GR 和 BDNF 的表达水平显著降低。相比之下,20E 的治疗,尤其是高浓度的治疗,逆转了糖尿病引起的上述情况。结果表明,20E 在拮抗糖尿病大鼠的记忆缺陷方面具有保护作用,可能是通过增强大脑的抗氧化能力。

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