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3-Hydroxybutyrate methyl ester as a potential drug against Alzheimer's disease via mitochondria protection mechanism

Alzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained... Full description

Journal Title: Biomaterials October 2013, Vol.34(30), pp.7552-7562
Main Author: Zhang, Junyu
Other Authors: Cao, Qian , Li, Shaowu , Lu, Xiaoyun , Zhao, Yongxi , Guan, Ji-Song , Chen, Jin-Chun , Wu, Qiong , Chen, Guo-Qiang
Format: Electronic Article Electronic Article
Language: English
Subjects:
Phb
ID: ISSN: 0142-9612 ; DOI: 10.1016/j.biomaterials.2013.06.043
Link: http://dx.doi.org/10.1016/j.biomaterials.2013.06.043
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recordid: sciversesciencedirect_elsevierS0142-9612(13)00758-8
title: 3-Hydroxybutyrate methyl ester as a potential drug against Alzheimer's disease via mitochondria protection mechanism
format: Article
creator:
  • Zhang, Junyu
  • Cao, Qian
  • Li, Shaowu
  • Lu, Xiaoyun
  • Zhao, Yongxi
  • Guan, Ji-Song
  • Chen, Jin-Chun
  • Wu, Qiong
  • Chen, Guo-Qiang
subjects:
  • 3-Hydroxybutyrate Methyl Ester
  • Alzheimer'S Disease
  • Mitochondria
  • Phb
ispartof: Biomaterials, October 2013, Vol.34(30), pp.7552-7562
description: Alzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained hypoglycemia. In this study, the derivative of 3HB, 3-hydroxybutyrate methyl ester (HBME), was used by cells as an alternative to glucose. HBME inhibited cell apoptosis under glucose deprivation, rescued activities of mitochondrial respiratory chain complexes that were impaired in AD patients and decreased the generation of ROS. Meanwhile, HBME stabilized the mitochondrial membrane potential. In vivo studies showed that HBME crossed the blood brain barrier easier compared with charged 3HB, resulting in a better bioavailability. AD mice treated with HBME performed significantly better (p 
language: eng
source:
identifier: ISSN: 0142-9612 ; DOI: 10.1016/j.biomaterials.2013.06.043
fulltext: fulltext
issn:
  • 01429612
  • 0142-9612
url: Link


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title3-Hydroxybutyrate methyl ester as a potential drug against Alzheimer's disease via mitochondria protection mechanism
creatorZhang, Junyu ; Cao, Qian ; Li, Shaowu ; Lu, Xiaoyun ; Zhao, Yongxi ; Guan, Ji-Song ; Chen, Jin-Chun ; Wu, Qiong ; Chen, Guo-Qiang
ispartofBiomaterials, October 2013, Vol.34(30), pp.7552-7562
identifierISSN: 0142-9612 ; DOI: 10.1016/j.biomaterials.2013.06.043
subject3-Hydroxybutyrate Methyl Ester ; Alzheimer'S Disease ; Mitochondria ; Phb
descriptionAlzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained hypoglycemia. In this study, the derivative of 3HB, 3-hydroxybutyrate methyl ester (HBME), was used by cells as an alternative to glucose. HBME inhibited cell apoptosis under glucose deprivation, rescued activities of mitochondrial respiratory chain complexes that were impaired in AD patients and decreased the generation of ROS. Meanwhile, HBME stabilized the mitochondrial membrane potential. In vivo studies showed that HBME crossed the blood brain barrier easier compared with charged 3HB, resulting in a better bioavailability. AD mice treated with HBME performed significantly better (p < 0.05) in the Morris water maze compared with other groups, demonstrating that HBME has a positive in vivo pharmaceutical effect to improve the spatial learning and working memory of mice. A reduced amyloid-β deposition in mouse brains after intragastric administration of HBME was also observed. Combined with the in vitro and in vivo results, HBME was proposed to be a drug candidate against AD, its working mechanism appeared to be mediated by various effects of protecting mitochondrial damages.
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descriptionAlzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained hypoglycemia. In this study, the derivative of 3HB, 3-hydroxybutyrate methyl ester (HBME), was used by cells as an alternative to glucose. HBME inhibited cell apoptosis under glucose deprivation, rescued activities of mitochondrial respiratory chain complexes that were impaired in AD patients and decreased the generation of ROS. Meanwhile, HBME stabilized the mitochondrial membrane potential. In vivo studies showed that HBME crossed the blood brain barrier easier compared with charged 3HB, resulting in a better bioavailability. AD mice treated with HBME performed significantly better (p < 0.05) in the Morris water maze compared with other groups, demonstrating that HBME has a positive in vivo pharmaceutical effect to improve the spatial learning and working memory of mice. A reduced amyloid-β deposition in mouse brains after intragastric administration of HBME was also observed. Combined with the in vitro and in vivo results, HBME was proposed to be a drug candidate against AD, its working mechanism appeared to be mediated by various effects of protecting mitochondrial damages.
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abstractAlzheimer's disease (AD) is induced by many reasons, including decreased cellular utilization of glucose and brain cell mitochondrial damages. Degradation product of microbially synthesized polyhydroxybutyrate (PHB), namely, 3-hydroxybutyrate (3HB), can be an alternative to glucose during sustained hypoglycemia. In this study, the derivative of 3HB, 3-hydroxybutyrate methyl ester (HBME), was used by cells as an alternative to glucose. HBME inhibited cell apoptosis under glucose deprivation, rescued activities of mitochondrial respiratory chain complexes that were impaired in AD patients and decreased the generation of ROS. Meanwhile, HBME stabilized the mitochondrial membrane potential. In vivo studies showed that HBME crossed the blood brain barrier easier compared with charged 3HB, resulting in a better bioavailability. AD mice treated with HBME performed significantly better (p < 0.05) in the Morris water maze compared with other groups, demonstrating that HBME has a positive in vivo pharmaceutical effect to improve the spatial learning and working memory of mice. A reduced amyloid-β deposition in mouse brains after intragastric administration of HBME was also observed. Combined with the in vitro and in vivo results, HBME was proposed to be a drug candidate against AD, its working mechanism appeared to be mediated by various effects of protecting mitochondrial damages.
pubElsevier Ltd
doi10.1016/j.biomaterials.2013.06.043
eissn18785905
date2013-10