Parkia biglobosaImproves Mitochondrial Functioning and Protects against Neurotoxic Agents in Rat Brain Hippocampal Slices
| Autor: | Fabiano B. Carvalho, João Rocha, Margareth Linde Athayde, Rodrigo Lopes Seeger, Kayode Komolafe, Akintunde A. Akindahunsi, Tolulope M. Olaleye, Cláudia Vargas Klimaczewski, Aline Augusti Boligon |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Mitochondrial ROS Article Subject Cell Survival Neurotoxins lcsh:Medicine Hippocampal formation Mitochondrion Pharmacology Hippocampus Parkia biglobosa General Biochemistry Genetics and Molecular Biology chemistry.chemical_compound medicine Animals Rats Wistar Membrane Potential Mitochondrial chemistry.chemical_classification Reactive oxygen species Dose-Response Relationship Drug General Immunology and Microbiology biology Plant Extracts lcsh:R Neurotoxicity Fabaceae Catechin General Medicine biology.organism_classification medicine.disease Mitochondria Rats Plant Leaves Dose–response relationship Neuroprotective Agents chemistry Biochemistry Reactive Oxygen Species Research Article |
| Zdroj: | BioMed Research International BioMed Research International, Vol 2014 (2014) |
| ISSN: | 2314-6141 2314-6133 |
| Popis: | Objective. Methanolic leaf extracts ofParkia biglobosa, PBE, and one of its major polyphenolic constituents, catechin, were investigated for their protective effects against neurotoxicity induced by different agents on rat brain hippocampal slices and isolated mitochondria.Methods. Hippocampal slices were preincubated with PBE (25, 50, 100, or 200 µg/mL) or catechin (1, 5, or 10 µg/mL) for 30 min followed by further incubation with 300 µM H2O2, 300 µM SNP, or 200 µM PbCl2for 1 h. Effects of PBE and catechin on SNP- or CaCl2-induced brain mitochondrial ROS formation and mitochondrial membrane potential (ΔΨm) were also determined.Results. PBE and catechin decreased basal ROS generation in slices and blunted the prooxidant effects of neurotoxicants on membrane lipid peroxidation and nonprotein thiol contents. PBE rescued hippocampal cellular viability from SNP damage and caused a significant boost in hippocampus Na+, K+-ATPase activity but with no effect on the acetylcholinesterase activity. Both PBE and catechin also mitigated SNP- or CaCl2-dependent mitochondrial ROS generation. Measurement by safranine fluorescence however showed that the mild depolarization of theΔΨmby PBE was independent of catechin.Conclusion. The results suggest that the neuroprotective effect of PBE is dependent on its constituent antioxidants and mild mitochondrial depolarization propensity. |
| Databáze: | OpenAIRE |
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