Spirulina Lipids Alleviate Oxidative Stress and Inflammation in Mice Fed a High-Fat and High-Sucrose Diet.

Yuhong Yang,Lei Du,Masashi Hosokawa,Kazuo Miyashita

doi:10.3390/md18030148

Abstract

High-fat and high-sucrose diet (HFHSD)-induced obesity leads to oxidative stress and chronic inflammatory status. However, little is known about the beneficial effects of total lipids extracted from Spirulina. Hence, in the present study, Spirulina lipids were extracted with chloroform/methanol (SLC) or ethanol (SLE) and then their effects on oxidative stress and inflammation in the mice fed a HFHSD were investigated. The results show that the major lipid classes and fatty acid profiles of SLC and SLE were almost similar, but the gamma-linolenic acid (GLA) and carotenoid contents in SLE was a little higher than that in SLC. Dietary 4% SLC or SLE for 12 weeks effectively decreased the hepatic lipid hydroperoxide levels as well as increased the activities and mRNA levels of antioxidant enzymes in the mice fed a HFHSD. In addition, supplementation with SLC and SLE also markedly decreased the levels of serum pro-inflammatory cytokines and the mRNA expression of pro-inflammatory cytokines in the liver and epididymal white adipose tissue of mice fed a HFHSD, and the effects of SLC and SLE were comparable. These findings confirm for the first time that dietary Spirulina lipids could alleviate HFHSD-induced oxidative stress and inflammation.

Highlights

Oxidative stress refers to an imbalance between excessive productions of reactive oxygen species (ROS) and their elimination by protective mechanisms [1]
It has been reported that many inflammation and macrophage-specific genes are dramatically upregulated in the white adipose tissue (WAT) of genetic and high-fat diet-induced obese mouse models [9]
The thin-layer chromatography (TLC) analysis showed that the major lipid classes of Spirulina lipids were extracted with chloroform/methanol (SLC) and Spirulina lipids extracted with ethanol (SLE) were GLs and phospholipids (PLs)

Summary

Introduction

Oxidative stress refers to an imbalance between excessive productions of reactive oxygen species (ROS) and their elimination by protective mechanisms [1]. Evidence suggests that oxidative stress is a critical factor for pathological obesity, which is considered a serious health burden worldwide because of its associated complications, such as diabetes, cardiovascular diseases, and hepatic steatosis [2,3]. It has been reported that ROS are selectively increased in the adipose tissue of obese individuals, together with the increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and the downregulation of antioxidative enzyme expression [4]. High-calorie diet induced obesity can induce systemic oxidative stress through various mechanisms, including superoxide generation from the NADPH oxidases, oxidative phosphorylation, glyceraldehyde auto-oxidation, protein kinase. It has been reported that many inflammation and macrophage-specific genes are dramatically upregulated in the white adipose tissue (WAT) of genetic and high-fat diet-induced obese mouse models [9]. Other studies have demonstrated that the development of obesity increases the

Results

Discussion

Conclusion