Sulforaphane protects against high cholesterol-induced mitochondrial bioenergetics impairments, inflammation, and oxidative stress and preserves pancreatic β-cells function

Carrasco-Pozo, Catalina, Tan, Kah Ni, Gotteland, Martin and Borges, Karin (2017) Sulforaphane protects against high cholesterol-induced mitochondrial bioenergetics impairments, inflammation, and oxidative stress and preserves pancreatic β-cells function. Oxidative Medicine and Cellular Longevity, 2017 3839756. doi:10.1155/2017/3839756


Author Carrasco-Pozo, Catalina
Tan, Kah Ni
Gotteland, Martin
Borges, Karin
Title Sulforaphane protects against high cholesterol-induced mitochondrial bioenergetics impairments, inflammation, and oxidative stress and preserves pancreatic β-cells function
Journal name Oxidative Medicine and Cellular Longevity   Check publisher's open access policy
ISSN 1942-0994
1942-0900
Publication date 2017-04-01
Year available 2017
Sub-type Article (original research)
DOI 10.1155/2017/3839756
Open Access Status DOI
Volume 2017
Start page 3839756
Total pages 15
Place of publication New York, NY, United States
Publisher Hindawi Limited
Language eng
Subject 1303 Biochemistry
1302 Ageing
1307 Cell Biology
Abstract Cholesterol plays an important role in inducing pancreatic β-cell dysfunction, leading to an impaired insulin secretory response to glucose. This study aimed to determine the protective effects of sulforaphane, a natural isothiocyanate Nrf2-inducer, against cholesterol-induced pancreatic β-cells dysfunction, through molecular and cellular mechanisms involving mitochondrial bioenergetics. Sulforaphane prevented cholesterol-induced alterations in the coupling efficiency of mitochondrial respiration, improving ATP turnover and spare capacity, and averted the impairment of the electron flow at complexes I, II, and IV. Sulforaphane also attenuated the cholesterol-induced activation of the NFB pathway, normalizing the expression of pro- and anti-inflammatory cytokines. In addition, it also inhibited the decrease in sirtuin 1 expression and greatly increased Pgc-1α expression in Min6 cells. Sulforaphane increased the expression of antioxidant enzymes downstream of the Nrf2 pathway and prevented lipid peroxidation induced by cholesterol. The antioxidant and anti-inflammatory properties of sulforaphane and its ability to protect and improve mitochondrial bioenergetic function contribute to its protective action against cholesterol-induced pancreatic β-cell dysfunction. Our data provide a scientifically tested foundation upon which sulforaphane can be developed as nutraceutical to preserve β-cell function and eventually control hyperglycemia.
Formatted abstract
Cholesterol plays an important role in inducing pancreatic β-cell dysfunction, leading to an impaired insulin secretory response to glucose. This study aimed to determine the protective effects of sulforaphane, a natural isothiocyanate Nrf2-inducer, against cholesterol-induced pancreatic β-cells dysfunction, through molecular and cellular mechanisms involving mitochondrial bioenergetics. Sulforaphane prevented cholesterol-induced alterations in the coupling efficiency of mitochondrial respiration, improving ATP turnover and spare capacity, and averted the impairment of the electron flow at complexes I, II, and IV. Sulforaphane also attenuated the cholesterol-induced activation of the NFB pathway, normalizing the expression of pro- and anti-inflammatory cytokines. In addition, it also inhibited the decrease in sirtuin 1 expression and greatly increased Pgc-1α expression in Min6 cells. Sulforaphane increased the expression of antioxidant enzymes downstream of the Nrf2 pathway and prevented lipid peroxidation induced by cholesterol. The antioxidant and anti-inflammatory properties of sulforaphane and its ability to protect and improve mitochondrial bioenergetic function contribute to its protective action against cholesterol-induced pancreatic β-cell dysfunction. Our data provide a scientifically tested foundation upon which sulforaphane can be developed as nutraceutical to preserve β-cell function and eventually control hyperglycemia.
Keyword Cell Biology
Cell Biology
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 11130232
1044007
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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