Sulforaphane Balances Ca2+ Homeostasis Injured by Excessive Fat via Mitochondria-Associated Membrane (MAM)

被引：23

作者：

Tian, Sicong ^{[1
]}

Lei, Peng ^{[2
]}

Zhang, Jing ^{[1
]}

Sun, Yao ^{[2
]}

Li, Baolong ^{[3
]}

Shan, Yujuan ^{[1
]}

机构：

[1] Wenzhou Med Univ, Sch Publ Hlth & Management, Wenzhou 325035, Peoples R China

[2] Harbin Inst Technol, Dept Food Sci & Engn, Sch Chem & Chem Engn, Harbin 150001, Peoples R China

[3] Heilongjiang Univ Chinese Med, Harbin 150040, Peoples R China

来源：

MOLECULAR NUTRITION & FOOD RESEARCH | 2021年 / 65卷 / 14期

基金：

中国国家自然科学基金;

关键词：

Ca2+ homeostasis; lipid metabolism; mitochondria-associated membrane; mitochondria function; sulforaphane; ENDOPLASMIC-RETICULUM; RECEPTOR;

D O I：

10.1002/mnfr.202001076

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Scope Mitochondria-associated membrane (MAM) connects endoplasmic reticulum (ER) and mitochondria plays a significant role in lipid metabolism and Ca2+ homeostasis. Albeit sulforaphane (SFN) shows potential in ameliorating excessive fat accumulation and mitochondrial function; whether MAM is a target of SFN and its underlying mechanisms are still unclear. Methods and Results High-fat-intake models are established both in vivo and in vitro. SFN widens the distance between ER and mitochondria and down-regulates MAM tether protein mitofusin-2. SFN reverses the increase of Ca2+ induced by fatty acid and inhibits the Ca2+ channel inositol-1,4,5-trisphosphate receptor (IP3R). Compared with high fat group, SFN alleviates Ca2+ overload in the mitochondria and suppresses mitochondrial calcium uniporter (MCU). Furthermore, SFN increases mitochondrial DNA quantities and mitochondria membrane potential, while decreasing reactive oxygen species (ROS) production. Finally, SFN increases mitochondria complexes IV content and ATP synthesis. Conclusion These results suggest that SFN balances the Ca2+ homeostasis in the MAM through regulating Ca2+ flux by Ca2+ channel IP3R and MCU.

引用

页数：9

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