Premium
Lycium barbarum Polysaccharide Supplementation Improves Alcoholic Liver Injury in Female Mice by Inhibiting Stearoyl‐CoA Desaturase 1
Author(s) -
Wang Fei,
Tipoe George L.,
Yang Changqing,
Nanji Amin A.,
Hao Xiangfeng,
So KwokFai,
Xiao Jia
Publication year - 2018
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800144
Subject(s) - ampk , alcoholic liver disease , liver injury , medicine , endocrinology , pharmacology , chemistry , lipid metabolism , fatty liver , ethanol , biochemistry , disease , protein kinase a , enzyme , cirrhosis
Scope Lycium barbarum polysaccharide (LBP) is a water fraction of wolfberry, which has been demonstrated to possess a hepatoprotective effect in several liver disease models. However, the anti‐alcoholic liver disease (anti‐ALD) mechanism of LBP has not been investigated thoroughly. Its protective effects on both male and femal mice are investigated in the current study. Methods and results A chronic ethanol‐fed ALD in vivo model is applied to study the effect of LBP in both male and female mice. It is observed that ethanol causes more severe liver injury in female than male mice, and the ameliorative effects of LBP are also more significant in female mice, which are impaired after complete bilateral oophorectomy. The hepatic SCD1 expression is found to be positively correlated with the severity of the liver damage and the main mediator of LBP inducer of protection. The AMPK‐CPT pathway is also activated by LBP to rebalance the dysregulated lipid metabolism during ALD development. By using concurrent sodium palmitate and an ethanol‐induced in vitro cell damage model in AML‐12 cell line, it is characterized that LBP directly interacts with ERα instead of ERβ to activate the SCD1‐AMPK‐CPT pathway. Conclusions LBP is an effective and safe hepatoprotective agent against ALD primarily through the SCD1‐AMPK‐CPT pathway after ERα agonist.