Parkia biglobosa Improves Mitochondrial Functioning and Protects against Neurotoxic Agents in Rat Brain Hippocampal Slices

• Published in: BioMed research international 2014-01, Vol.2014 (2014), p.1-15
• Main Authors: Komolafe, Kayode, Olaleye, Tolulope M., Seeger, Rodrigo L., Carvalho, Fabiano B., Augusti Boligon, Aline, Athayde, Margareth Linde, Klimaczewski, Claudia V., Akindahunsi, Akintunde A., Rocha, Joao B. T.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Beans; Biomedical research; Cell Survival - drug effects; Dose-Response Relationship, Drug; Enzymes; Fabaceae - chemistry; Free radicals; Health aspects; Hippocampus (Brain); Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - pathology; Legumes; Male; Materia medica, Vegetable; Membrane Potential, Mitochondrial - drug effects; Membrane Potential, Mitochondrial - physiology; Mimosaceae; Mitochondria; Mitochondria - drug effects; Mitochondria - physiology; Natural products; Neuroprotective Agents - administration & dosage; Neurotoxicity syndromes; Neurotoxins - toxicity; Oxidative stress; Parkia biglobosa; Plant extracts; Plant Extracts - administration & dosage; Plant Leaves - chemistry; Potassium; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Rodents; Studies
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2014/326290

Objective. Methanolic leaf extracts of Parkia 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 PbCl2 for 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 the ΔΨm by 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.