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Propolis is a resin produced by bees from raw material collected from plants, salivary secretions, and beeswax. New therapeutic properties for the Central Nervous System have emerged. We explored the neurobehavioral and antioxidant effects of an ethanolic extract of yellow propolis (EEYP) rich in triterpenoids, primarily lupeol and -amyrin. Male Wistar rats, 3 months old, were intraperitoneally treated with Tween 5% (control), EEYP (1, 3, 10, and 30 mg/kg), or diazepam, fluoxetine, and caffeine (positive controls) 30 min before the assays. Animals were submitted to open field, elevated plus maze, forced swimming, and inhibitory avoidance tests. After behavioral tasks, blood samples were collected through intracardiac pathway, to evaluate the oxidative balance. The results obtained in the open field and in the elevated plus maze assay showed spontaneous locomotion preserved and anxiolytic-like activity. In the forced swimming test, EEYP demonstrated antidepressant-like activity. In the inhibitory avoidance test, EEYP showed mnemonic activity at 30 mg/kg. In the evaluation of oxidative biochemistry, the extract reduced the production of nitric oxide and malondialdehyde without changing level of total antioxidant, catalase, and superoxide dismutase, induced by behavioral stress. Our results highlight that EEYP emerges as a promising anxiolytic, antidepressant, mnemonic, and antioxidant natural product.
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http://dx.doi.org/10.1155/2016/2906953 | DOI Listing |
Toxics
August 2025
Institute of Environmental Systems Biology, College of Environment Science and Engineering, Dalian Maritime University, Linghai Road 1, Dalian 116026, China.
Sodium p-perfluorous nonenoxybenzenesulfonate (OBS) has been proposed as a substitute for perfluorooctanesulfonic acid (PFOS), yet it has garnered increasing attention due to its environmental persistence and potential toxicity. Despite these concerns, the neurotoxic mechanisms of OBS remain unclear. This study investigates and compares the neurotoxic effects and mechanisms of OBS and PFOS in .
View Article and Find Full Text PDFToxicon
August 2025
Neuroanatomy and Neurotrauma Research Laboratories, Department of Anatomy, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Oyo State, 20005, Nigeria.
Aflatoxin B (AFB) is a mycotoxin known for its liver toxicity and cancer risk, as well as neurotoxic effects causing motor and cognitive issues in humans and animals. Ongoing research into protecting against AFB damage has recently focused on antioxidant and anti-inflammatory agents. Gallic acid (GA), a low molecular weight triphenolic acid, demonstrates notable anti-oxidative and anti-inflammatory activities.
View Article and Find Full Text PDFAssay Drug Dev Technol
August 2025
L.J. Institute of Pharmacy, LJ University, Ahmedabad, India.
Biochim Biophys Acta Mol Basis Dis
August 2025
Neurophysiology Laboratory, Neurosurgical Service, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan. Electronic address:
Background: Remote ischemic preconditioning (RIPC) is a protective strategy in which transient ischemia and reperfusion in one organ confers protection to another. This can be mediated by humoral responses, transcriptional processes, or both. These protective effects are hypothesized to result from enhanced cellular tolerance to ischemia.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
August 2025
Radiation Biology Research Department, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt.
Objectives: Cannabidiol (CBD), the primary component of Cannabis sativa, has a neuroprotective and anti-inflammatory properties. Due to its modulation of multiple molecular targets within the central nervous system, CBD holds therapeutic promise for various neurological and psychiatric disorders.
Methods: This study aimed to evaluate the potential protective effects of CBD and/or low-dose ionizing radiation (LDR) in a rat model of hepatic encephalopathy (HE) induced by thioacetamide (TAA).