C-phycoerythrin from Phormidium persicinum Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress
| Autor: | Andrea Augusto Sfriso, Placido Rojas-Franco, Cristian Garcia-Hernandez, Jose Ivan Serrano-Contreras, Vanessa Blas-Valdivia, Edgar Cano-Europa, Margarita Franco-Colín |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
Programmed cell death Aquatic Organisms Phormidium persicinum mercury QH301-705.5 Medicinal & Biomolecular Chemistry Pharmaceutical Science Oxidative phosphorylation medicine.disease_cause Cyanobacteria Protective Agents Article NO Mice Drug Discovery medicine Animals Humans oxidative stress Biology (General) Protein kinase A C-phycoerythrin Pharmacology Toxicology and Pharmaceutics (miscellaneous) Cell damage 0306 Physical Chemistry (incl. Structural) biology Chemistry Endoplasmic reticulum Phycoerythrin medicine.disease Cell biology Disease Models Animal acute kidney injury Mercuric Chloride Rhodophyta Unfolded protein response Podocin biology.protein endoplasmic reticulum stress 1115 Pharmacology and Pharmaceutical Sciences Acute kidney injury Endoplasmic reticulum stress Mercury Oxidative stress |
| Zdroj: | Marine Drugs Volume 19 Issue 11 Marine Drugs, Vol 19, Iss 589, p 589 (2021) |
| ISSN: | 1660-3397 |
| DOI: | 10.3390/md19110589 |
| Popis: | C-phycoerythrin (C-PE) is a phycobiliprotein that prevents oxidative stress and cell damage. The aim of this study was to evaluate whether C-PE also counteracts endoplasmic reticulum (ER) stress as a mechanism contributing to its nephroprotective activity. After C-PE was purified from Phormidium persicinum by using size exclusion chromatography, it was characterized by spectrometry and fluorometry. A mouse model of HgCl2-induced acute kidney injury (AKI) was used to assess the effect of C-PE treatment (at 25, 50, or 100 mg/kg of body weight) on oxidative stress, the redox environment, and renal damage. ER stress was examined with the same model and C-PE treatment at 100 mg/kg. C-PE diminished oxidative stress and cell damage in a dose-dependent manner by impeding the decrease in expression of nephrin and podocin normally caused by mercury intoxication. It reduced ER stress by preventing the activation of the inositol-requiring enzyme-1α (IRE1α) pathway and avoiding caspase-mediated cell death, while leaving the expression of protein kinase RNA-like ER kinase (PERK) and activating transcription factor 6α (ATF6α) pathways unmodified. Hence, C-PE exhibited a nephroprotective effect on HgCl2-induced AKI by reducing oxidative stress and ER stress. |
| Databáze: | OpenAIRE |
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