Cytoprotective effects of hesperetin and hesperidin against amyloid β-induced impairment of glucose transport through downregulation of neuronal autophagy

Shang Ming Huang, Shin Yi Tsai, Jer An Lin, Chi Hao Wu, Gow Chin Yen

研究成果: 雜誌貢獻文章

37 引文 (Scopus)

摘要

Scope: This study investigated whether flavonoids, such as hesperetin and hesperidin, inhibited amyloid β (Aβ)-impaired glucose utilization through regulating cellular autophagy in insulin-stimulated neuronal cells. Methods and results: In this study, we used a toxic Aβ1-42 peptide to impair insulin-stimulated glucose utilization in Neuro-2A cells, and this study also hypothesized that Aβ-induced autophagy might be emerging as a key process regulating neuronal glucose uptake. Additionally, hesperetin and hesperidin were used to test the neuroprotective effect against Aβ-induced impairment of glucose utilization. Our data found that Aβ-stimulated autophagy activation promoted the phenomenon of impairment of neuronal energy metabolism, including glucose uptake, glucose transporters (GLUTs), and insulin signaling cascades. In this study, confocal images of autophagy punctate further confirmed that downregulation of Aβ-stimulated autophagy could increase insulin-stimulated neuronal glucose uptake. Moreover, treatment with hesperetin and hesperidin improved Aβ-impaired glucose utilization by inhibiting Aβ-induced autophagy in neuronal cells. Conclusion: These findings suggest that downregulation of autophagy may be one of the approaches to control the impairment of energy metabolism leading to neuronal injury in the early development of Alzheimer's disease, and hesperetin or hesperidin may be a potential agent in the preventing of Alzheimer's disease progression.

原文英語
頁(從 - 到)601-609
頁數9
期刊Molecular Nutrition and Food Research
56
發行號4
DOIs
出版狀態已發佈 - 四月 2012
對外發佈Yes

指紋

Hesperidin
hesperetin
hesperidin
autophagy
Autophagy
amyloid
Amyloid
Down-Regulation
Glucose
glucose
insulin
Insulin
Alzheimer disease
uptake mechanisms
energy metabolism
Energy Metabolism
Alzheimer Disease
neurons
neuroprotective effect
glucose transporters

ASJC Scopus subject areas

  • Food Science
  • Biotechnology

引用此文

Cytoprotective effects of hesperetin and hesperidin against amyloid β-induced impairment of glucose transport through downregulation of neuronal autophagy. / Huang, Shang Ming; Tsai, Shin Yi; Lin, Jer An; Wu, Chi Hao; Yen, Gow Chin.

於: Molecular Nutrition and Food Research, 卷 56, 編號 4, 04.2012, p. 601-609.

研究成果: 雜誌貢獻文章

@article{9a2c1796618b458b91d95b52df658769,
title = "Cytoprotective effects of hesperetin and hesperidin against amyloid β-induced impairment of glucose transport through downregulation of neuronal autophagy",
abstract = "Scope: This study investigated whether flavonoids, such as hesperetin and hesperidin, inhibited amyloid β (Aβ)-impaired glucose utilization through regulating cellular autophagy in insulin-stimulated neuronal cells. Methods and results: In this study, we used a toxic Aβ1-42 peptide to impair insulin-stimulated glucose utilization in Neuro-2A cells, and this study also hypothesized that Aβ-induced autophagy might be emerging as a key process regulating neuronal glucose uptake. Additionally, hesperetin and hesperidin were used to test the neuroprotective effect against Aβ-induced impairment of glucose utilization. Our data found that Aβ-stimulated autophagy activation promoted the phenomenon of impairment of neuronal energy metabolism, including glucose uptake, glucose transporters (GLUTs), and insulin signaling cascades. In this study, confocal images of autophagy punctate further confirmed that downregulation of Aβ-stimulated autophagy could increase insulin-stimulated neuronal glucose uptake. Moreover, treatment with hesperetin and hesperidin improved Aβ-impaired glucose utilization by inhibiting Aβ-induced autophagy in neuronal cells. Conclusion: These findings suggest that downregulation of autophagy may be one of the approaches to control the impairment of energy metabolism leading to neuronal injury in the early development of Alzheimer's disease, and hesperetin or hesperidin may be a potential agent in the preventing of Alzheimer's disease progression.",
keywords = "Amyloid β, Autophagy, Glucose uptake, Hesperetin, Hesperidin",
author = "Huang, {Shang Ming} and Tsai, {Shin Yi} and Lin, {Jer An} and Wu, {Chi Hao} and Yen, {Gow Chin}",
year = "2012",
month = "4",
doi = "10.1002/mnfr.201100682",
language = "English",
volume = "56",
pages = "601--609",
journal = "Molecular Nutrition and Food Research",
issn = "1613-4125",
publisher = "Wiley-VCH Verlag",
number = "4",

}

TY - JOUR

T1 - Cytoprotective effects of hesperetin and hesperidin against amyloid β-induced impairment of glucose transport through downregulation of neuronal autophagy

AU - Huang, Shang Ming

AU - Tsai, Shin Yi

AU - Lin, Jer An

AU - Wu, Chi Hao

AU - Yen, Gow Chin

PY - 2012/4

Y1 - 2012/4

N2 - Scope: This study investigated whether flavonoids, such as hesperetin and hesperidin, inhibited amyloid β (Aβ)-impaired glucose utilization through regulating cellular autophagy in insulin-stimulated neuronal cells. Methods and results: In this study, we used a toxic Aβ1-42 peptide to impair insulin-stimulated glucose utilization in Neuro-2A cells, and this study also hypothesized that Aβ-induced autophagy might be emerging as a key process regulating neuronal glucose uptake. Additionally, hesperetin and hesperidin were used to test the neuroprotective effect against Aβ-induced impairment of glucose utilization. Our data found that Aβ-stimulated autophagy activation promoted the phenomenon of impairment of neuronal energy metabolism, including glucose uptake, glucose transporters (GLUTs), and insulin signaling cascades. In this study, confocal images of autophagy punctate further confirmed that downregulation of Aβ-stimulated autophagy could increase insulin-stimulated neuronal glucose uptake. Moreover, treatment with hesperetin and hesperidin improved Aβ-impaired glucose utilization by inhibiting Aβ-induced autophagy in neuronal cells. Conclusion: These findings suggest that downregulation of autophagy may be one of the approaches to control the impairment of energy metabolism leading to neuronal injury in the early development of Alzheimer's disease, and hesperetin or hesperidin may be a potential agent in the preventing of Alzheimer's disease progression.

AB - Scope: This study investigated whether flavonoids, such as hesperetin and hesperidin, inhibited amyloid β (Aβ)-impaired glucose utilization through regulating cellular autophagy in insulin-stimulated neuronal cells. Methods and results: In this study, we used a toxic Aβ1-42 peptide to impair insulin-stimulated glucose utilization in Neuro-2A cells, and this study also hypothesized that Aβ-induced autophagy might be emerging as a key process regulating neuronal glucose uptake. Additionally, hesperetin and hesperidin were used to test the neuroprotective effect against Aβ-induced impairment of glucose utilization. Our data found that Aβ-stimulated autophagy activation promoted the phenomenon of impairment of neuronal energy metabolism, including glucose uptake, glucose transporters (GLUTs), and insulin signaling cascades. In this study, confocal images of autophagy punctate further confirmed that downregulation of Aβ-stimulated autophagy could increase insulin-stimulated neuronal glucose uptake. Moreover, treatment with hesperetin and hesperidin improved Aβ-impaired glucose utilization by inhibiting Aβ-induced autophagy in neuronal cells. Conclusion: These findings suggest that downregulation of autophagy may be one of the approaches to control the impairment of energy metabolism leading to neuronal injury in the early development of Alzheimer's disease, and hesperetin or hesperidin may be a potential agent in the preventing of Alzheimer's disease progression.

KW - Amyloid β

KW - Autophagy

KW - Glucose uptake

KW - Hesperetin

KW - Hesperidin

UR - http://www.scopus.com/inward/record.url?scp=84859769676&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84859769676&partnerID=8YFLogxK

U2 - 10.1002/mnfr.201100682

DO - 10.1002/mnfr.201100682

M3 - Article

C2 - 22383310

AN - SCOPUS:84859769676

VL - 56

SP - 601

EP - 609

JO - Molecular Nutrition and Food Research

JF - Molecular Nutrition and Food Research

SN - 1613-4125

IS - 4

ER -