Protective effects of fusidic acid against sodium nitroprusside-induced apoptosis in C6 glial cells
| Autor: | Euteum Park, Do Kyung Kim, Hong Sung Chun, Jae-Sung Kim, Seung Kim, Chun-Sung Kim |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Nitroprusside
0301 basic medicine Antioxidant medicine.medical_treatment Fusidic acid Apoptosis Pharmacology Cell Line Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals chemistry.chemical_classification Reactive oxygen species General Neuroscience AMPK Endoplasmic Reticulum Stress Anti-Bacterial Agents Rats Neuroprotective Agents 030104 developmental biology chemistry Sodium nitroprusside Fusidic Acid Neuroglia 030217 neurology & neurosurgery Peroxynitrite medicine.drug |
| Zdroj: | NeuroReport. 30:1222-1229 |
| ISSN: | 0959-4965 |
| Popis: | Fusidic acid, a steroidal antibiotic, possesses antimicrobial, antioxidant, and anti-inflammatory properties, but the effect of fusidic acid against neurodegenerative disease-related cell death has not been studied. Here, we investigated the protective effects of fusidic acid on sodium nitroprusside (SNP)-induced toxicity in C6 glial cells. Fusidic acid (5-20 μM) prevented SNP (100 μM)-induced cell death dose dependently, and effectively attenuated SNP-induced generation of nitric oxide (NO), total reactive oxygen species (ROS), and peroxynitrite (ONOO). Fusidic acid (20 μM) pretreatment significantly suppressed SNP (100 μM)-induced apoptotic events, such as nuclear condensation and caspase-3 activation. In addition, fusidic acid effectively attenuated SNP-induced endoplasmic reticulum (ER) stress markers, such as GRP78, IRE1, ATF6, PERK, XBP1s, eIF2α, CHOP, and caspase-12. A specific adenosine monophosphate-activated protein kinase (AMPK) inhibitor, compound C (10 μM), reversed the preventive effects of fusidic acid against SNP-induced cytotoxicity, CHOP elevation, and caspase-3 activation. These results suggest that fusidic acid can protect C6 glial cells against cytotoxicity, through the regulation of AMPK pathway and apoptotic events. |
| Databáze: | OpenAIRE |
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