Abstract
High-density lipoproteins (HDLs) play an important role in reverse cholesterol transport and present antioxidant properties, among others. In the central nervous system (CNS), there are HDLs, where these lipoproteins could influence brain health. Owing to the new evidence of HDL functionality remodeling in obese patients, and the fact that obesity-associated metabolic disturbances is pro-inflammatory and pro-oxidant, the aim of this study was to investigate if HDL functions are depleted in obese patients and obesity-associated microenvironment. HDLs were isolated from normal-weight healthy (nwHDL) and obese men (obHDL). The oxHDL level was measured by malondialdehyde and 4-hydroxynoneal peroxided products. BV2 microglial cells were exposed to different concentrations of nwHDL and obHDL in different obesity-associated pro-inflammatory microenvironments. Our results showed that hyperleptinemia increased oxHDL levels. In addition, nwHDLs reduced pro-inflammatory cytokines’ release and M1 marker gene expression in BV2 microglial cells. Nevertheless, both nwHDL co-administered with LPS+leptin and obHDL promoted BV2 microglial activation and a higher pro-inflammatory cytokine production, thus confirming that obesity-associated metabolic disturbances reverse the antioxidant and anti-inflammatory properties of HDLs in microglial cells.
Highlights
High-density lipoproteins (HDLs) are circulating particles; beyond serving as lipid transporters, they carry out a wide number of biological functions [1]
HDL-C was slightly lower in participants with obesity compared to those with a normal weight (p = 0.111)
HDLs and leptin in the central nervous system. The purpose of this project was to establish whether HDL and leptin may act as mediators of microglial plasticity and influence neuroinflammation
Summary
High-density lipoproteins (HDLs) are circulating particles; beyond serving as lipid transporters, they carry out a wide number of biological functions [1]. The fundamental activity of HDLs is cholesterol transport from peripheral tissues to the liver for catabolism and excretion into the bile. In physiological conditions, HDLs have been recently reported to exert other functions, including anti-inflammatory and antioxidant capacity, highly dependent on HDL composition [2]. The antioxidant capacity of HDLs is mainly conferred by the presence of apolipoproteins and enzymes transported by HDLs, including paraoxonase 1 (PON1) [3]. Lipid components are essential in HDL-related antioxidant capacity in order to prevent their own oxidation and low-density lipoproteins (LDLs) oxidation [4]. The oxidation of HDLs occurs in different pathological conditions characterized by an oxidant microenvironment increased, such as
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