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Shrimp Lipid Prevents Endoplasmic Reticulum-Mediated Endothelial Cell Damage
Zin Zin Ei1, Soottawat Benjakul2, Natchaphol Buamard2
1Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand.
Abstract:
Shrimp contains a fat that benefits cardiovascular function and may help in the prevention of diseases. The stress of essential cellular organelle endoplasmic reticulum (ER) is linked to endothelial dysfunction and damage. This research aimed at investigating the effect of shrimp lipid (SL) on endothelial cells in response to ER stress, as well as the underlying mechanisms. Human endothelial cells were pretreated with SL (250 and 500 μg/mL) for 24 h, and treated with 0.16 μg/mL of Thapsigargin (Tg) for 24 h. The apoptosis and necrosis were detected by Hoechst 33342/propidium iodide (PI) co-staining. Cellular signaling pathways and ER stress markers were evaluated by Western blot analysis and immunofluorescence. SL protected against ER-induced endothelial cell apoptosis. According to the results, the viability of EA.hy926 cells treated with Tg alone was 44.97 ± 1%, but SL (250 μg/mL) pretreatment increased cell viability to 77.26 ± 3.9%, and SL (500 μg/mL) increased to 72.42 ± 4.3%. SL suppressed the increase in ER stress regulator glucose-regulated protein 78 (GRP78) and attenuated the RNA-dependent protein kinase-like ER eukaryotic initiation factor-2α kinase (PERK) and inositol-requiring ER-to-nucleus signaling protein 1 (IRE1) pathways. SL could inhibit cell damage by reducing the ER-related apoptosis protein, C/EBPα-homologous protein (CHOP), induced by ER stress. Taken together, we found the protective effect and mechanism of SL in protecting ER stress-induced endothelial cell apoptosis through suppression of the ER stress pathway. The findings may support the potential use of SL as an approach with a protective effect on endothelial cells.
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