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萝卜硫素可预防糖尿病大鼠的神经元凋亡和记忆损伤。

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats.

作者信息

Wang Gengyin, Fang Hui, Zhen Yanfeng, Xu Gang, Tian Jinli, Zhang Yazhong, Zhang Dandan, Zhang Guyue, Xu Jing, Zhang Zhiyue, Qiu Mingyue, Ma Yijia, Zhang Hongrui, Zhang Xinxin

机构信息

Department of Internal Medicine, Hebei Medical University, Shijiazhuang, China.

出版信息

Cell Physiol Biochem. 2016;39(3):901-7. doi: 10.1159/000447799. Epub 2016 Aug 9.

Abstract

BACKGROUND/AIMS: To explore the effects of sulforaphane (SFN) on neuronal apoptosis in hippocampus and memory impairment in diabetic rats.

METHODS

Thirty male rats were randomly divided into normal control, diabetic model and SFN treatment groups (N = 10 in each group). Streptozotocin (STZ) was applied to establish diabetic model. Water Morris maze task was applied to test learning and memory. Tunel assaying was used to detect apoptosis in hippocampus. The expressions of Caspase-3 and myeloid cell leukemia 1(MCL-1) were detected by western blotting. Neurotrophic factor levels and AKT/GSK3β pathway were also detected.

RESULTS

Compared with normal control, learning and memory were apparently impaired, with up-regulation of Caspase-3 and down-regulation of MCL-1 in diabetic rats. Apoptotic neurons were also found in CA1 region after diabetic modeling. By contrast, SFN treatment prevented the memory impairment, decreased the apoptosis of hippocampal neurons. SFN also attenuated the abnormal expression of Caspase-3 and MCL-1 in diabetic model. Mechanically, SFN treatment reversed diabetic modeling-induced decrease of p-Akt, p-GSK3β, NGF and BDNF expressions.

CONCLUSION

SFN could prevent the memory impairment and apoptosis of hippocampal neurons in diabetic rat. The possible mechanism was related to the regulation of neurotropic factors and Akt/GSK3β pathway.

摘要

背景/目的:探讨萝卜硫素(SFN)对糖尿病大鼠海马神经元凋亡及记忆损伤的影响。

方法

将30只雄性大鼠随机分为正常对照组、糖尿病模型组和SFN治疗组(每组10只)。应用链脲佐菌素(STZ)建立糖尿病模型。采用水迷宫任务测试学习和记忆能力。运用Tunel检测法检测海马组织中的细胞凋亡情况。通过蛋白质印迹法检测Caspase-3和髓系细胞白血病-1(MCL-1)的表达。同时检测神经营养因子水平及AKT/GSK3β信号通路。

结果

与正常对照组相比,糖尿病大鼠的学习和记忆能力明显受损,Caspase-3表达上调,MCL-1表达下调。糖尿病建模后在CA1区也发现了凋亡神经元。相比之下,SFN治疗可预防记忆损伤,减少海马神经元凋亡。SFN还可减轻糖尿病模型中Caspase-3和MCL-1的异常表达。机制上,SFN治疗可逆转糖尿病建模诱导的p-Akt、p-GSK3β、神经生长因子(NGF)和脑源性神经营养因子(BDNF)表达降低。

结论

SFN可预防糖尿病大鼠的记忆损伤和海马神经元凋亡。其可能机制与神经营养因子及Akt/GSK3β信号通路的调节有关。

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