Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

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 app...

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Veröffentlicht in:Cellular physiology and biochemistry 2016-01, Vol.39 (3), p.901-907
Hauptverfasser: 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
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container_issue 3
container_start_page 901
container_title Cellular physiology and biochemistry
container_volume 39
creator 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
description 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.
doi_str_mv 10.1159/000447799
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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. 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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. 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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.</abstract><cop>Basel, Switzerland</cop><pub>Cell Physiol Biochem Press GmbH &amp; Co KG</pub><pmid>27497670</pmid><doi>10.1159/000447799</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Anticarcinogenic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Brain-Derived Neurotrophic Factor - genetics
Brain-Derived Neurotrophic Factor - metabolism
Caspase 3 - genetics
Caspase 3 - metabolism
Cognitive Dysfunction - physiopathology
Cognitive Dysfunction - prevention & control
Diabetes
Diabetes Mellitus, Experimental - chemically induced
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - genetics
Diabetes Mellitus, Experimental - physiopathology
Drug Repositioning
Gene Expression - drug effects
Glycogen Synthase Kinase 3 beta - genetics
Glycogen Synthase Kinase 3 beta - metabolism
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
Hypoglycemic Agents - pharmacology
Isothiocyanates - pharmacology
Male
Maze Learning - drug effects
Memory - drug effects
Memory impairment
Myeloid Cell Leukemia Sequence 1 Protein - genetics
Myeloid Cell Leukemia Sequence 1 Protein - metabolism
Nerve Growth Factor - genetics
Nerve Growth Factor - metabolism
Neurons - drug effects
Neurons - metabolism
Neurons - pathology
Original Paper
Proto-Oncogene Proteins c-akt - genetics
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Sprague-Dawley
Streptozocin
Sulforaphane
title Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats
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