Antioxidant Profile of 1‐Monocaffeoyl Glycerol in Lipophobic/Lipophilic Media

Abstract

Oxidative stress has been generally considered as one trigger of organism imbalance, resulting in lipid peroxidation, DNA damage and protein oxidation, which could be relieved by antioxidant supplement or endogenous antioxidant system. In present study, 1‐monocaffeoyl glycerol (1‐MCG), an amphipathic caffeic acid natural derivative, was enzymatically synthesized by Lipozyme 435, and its antioxidant profile in both lipophilic and lipophobic media was evaluated. The 1‐MCG was identified by HPLC‐UV, HPLC‐ESI‐MS, and 1H/13C‐NMR. Subsequently, antioxidant assays in lipophilic (DPPH assay) and lipophobic (ABTS, ORAC, erythrocyte hemolysis, ROS, MDA, and GPx assays) systems were explored. The better and lasting DPPH· and ABTS+· inhibitions of 1‐MCG than caffeic acid (CA) were related to its better solubilities in ethanol/water media and electron transfer ability. ORAC results suggested the radical scavenging activities of 1‐MCG (5 to 40 µM) were higher than Trolox. Furthermore, the effectiveness of 1‐MCG against AAPH‐induced erythrocytes oxidation indicated that 1‐MCG can effectively inhibit hemolysis. ESEM was also applied to verify the hemolysis inhibition and morphology preservation abilities of 1‐MCG. Besides, results showed 1‐MCG was able to prevent ROS from invasion, reduce production of MDA, up‐regulated GPx activity, terminate lipid peroxidation, and maintain the integrity of the structure and function of erythrocytes. Practical Application As an amphiphilic caffeic acid derivative, 1‐monocaffeoyl glycerol was synthesized, purified, and identified. 1‐Monocaffeoyl glycerol could significantly eliminate radicals including DPPH·, ABTS+·, and AAPH in ethanol, water, and PBS system, respectively. 1‐Monocaffeoyl glycerol could protect erythrocyte from AAPH induced hemolysis.

Hypothalamic JNK1-hepatic fatty acid synthase axis mediates a metabolic rewiring that prevents hepatic steatosis in male mice treated with olanzapine via intraperitoneal: Additional effects of PTP1B inhibition

“…To test this, metabolomic and lipidomic studies of the hypothalamus were performed. A detailed analysis of a broad spectrum of small molecular weight metabolites revealed a significant decrease in those with antioxidant properties such as choline, glycine, acetate, N-acetylaspartate and sn-Glycero-3-phosphocholine [ [74] , [75] , [76] , [77] , [78] , [79] , [80] , [81] , [82] , [83] ] in the hypothalamus of OLA-treated WT male mice in comparison to the control mice receiving VEH, whereas no statistically differences were found in the levels of these metabolites in the hypothalamus of PTP1B–KO mice ( Fig. 5 A).…”

“…It is noteworthy to highlight that our results herein show for the first time that the hypothalamic JNK activation in OLA-treated WT male mice via i.p. correlated with a marked reduction in antioxidant mediators in this brain region [ [74] , [75] , [76] , [77] , [78] , [79] , [80] , [81] , [82] , [83] ] which, in turn, increases protein nitration and lipid peroxidation, pointing to an increase in ROS levels and augmented oxidative stress in the hypothalamus during chronic OLA treatment by this administration route. These results in vivo were supported by the increase in MitoTracker Red CM-H 2 Xros staining observed in GT1-7 hypothalamic neurons treated directly with OLA.…”