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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4142556PMC
http://dx.doi.org/10.1155/2014/326290DOI Listing

Publication Analysis

Top Keywords

hippocampal slices
12
pbe catechin
12
parkia biglobosa
8
agents rat
8
rat brain
8
brain hippocampal
8
pbe
8
mitochondrial ros
8
ros generation
8
mitochondrial
5

Similar Publications

Excitatory synapses and the actin-rich dendritic spines on which they reside are indispensable for information processing and storage in the brain. In the adult hippocampus, excitatory synapses must balance plasticity and stability to support learning and memory. However, the mechanisms governing this balance remain poorly understood.

View Article and Find Full Text PDF

Differential suppression of hippocampal network oscillations by neuropeptide Y.

Neuropharmacology

December 2024

Institute of Physiology and Pathophysiology, Heidelberg University, Im Neuenheimer Feld 326, 69120 Heidelberg, Germany.

Neuropeptide Y (NPY) is the most abundant neuropeptide in the brain. It exerts anxiolytic and anticonvulsive actions, reduces stress and suppresses fear memory. While its effects at the behavioral and cellular levels have been well studied, much less is known about the modulation of physiological activity patterns at the network level.

View Article and Find Full Text PDF

Objective: Hypoxic-ischemic brain damage (HIBD) is a leading cause of neonatal mortality, resulting in brain injury and persistent seizures that can last into the late neonatal period and beyond. Effective treatments and interventions for infants affected by hypoxia-ischemia remain lacking. Clinical investigations have indicated an elevation of nuclear factor of activated T cells 5 (NFAT5) in whole blood from umbilical cords of severely affected HIBD infants with epilepsy.

View Article and Find Full Text PDF

Towards an Understanding of the Dentate Gyrus Hilus.

Hippocampus

January 2025

Department of Child and Adolescent Psychology, Neuroscience & Physiology, and Psychiatry and the Neuroscience Institute, New York University Grossman School of Medicine, New York University Langone Health, New York, New York, USA.

For many years, the hilus of the dentate gyrus (DG) was a mystery because anatomical data suggested a bewildering array of cells without clear organization. Moreover, some of the anatomical information led to more questions than answers. For example, it had been identified that one of the major cell types in the hilus, the mossy cell, innervates granule cells (GCs).

View Article and Find Full Text PDF

Discovery of MDI-114215: A Potent and Selective LIMK Inhibitor To Treat Fragile X Syndrome.

J Med Chem

December 2024

Medicines Discovery Institute, School of Biosciences, Cardiff University, Main Building, Park Place, Cardiff CF10 3AT, U.K.

LIMKs are serine/threonine and tyrosine kinases responsible for controlling cytoskeletal dynamics as key regulators of actin stability, ensuring synaptic health through normal synaptic bouton structure and function. However, LIMK1 overactivation results in abnormal dendritic synaptic development that characterizes the pathogenesis of Fragile X Syndrome (FXS). As a result, the development of LIMK inhibitors represents an emerging disease-modifying therapeutic approach for FXS.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!