chrysin and Brain-Injuries--Traumatic

Brain disorders are currently one of the world's most serious and difficult health issues. These brain disorders are accountable for a massive number of morbidities and mortalities around the world. The current treatments of these disorders are frequently accompanied by severe side effects and cause a detrimental effect on health. Recently, plant flavonoids have sparked a surge in public and scientific attention because of their alleged health-promoting impact and almost no adverse repercussions. Also, scientific research has shown that phytochemicals possess numerous neuroprotective properties under in vivo and in vitro conditions. Chrysin is a therapeutic phytochemical that falls under the class of flavonoids based on its structure. The biological activities and pharmacological effects of chrysin include anticancer, antioxidant, and anti-inflammatory activities as well as amyloidogenic and neurotrophic effects. These therapeutic abilities of chrysin are attributed to its structural diverseness arising in ring-A and lack of oxygenation in B and C rings. Several studies have highlighted the rising significance of chrysin in a variety of brain illnesses, like Alzheimer's disease, Parkinson's disease, depression, anxiety, brain tumours, epilepsy, multiple sclerosis, traumatic brain injury, spinal cord injury, and ischemic stroke. This study depicts the relationship of chrysin with different brain-related disorders and discusses the mechanisms responsible for the potential role of chrysin as a pharmacological agent for the treatment and management of different brain disorders based on the results of several preclinical studies and taking into account the therapeutic effects of the compound.

Topics: Antioxidants; Brain; Brain Injuries, Traumatic; Flavonoids; Humans

Traumatic brain injury (TBI) is recognized as an important risk factor for cognitive deficits. The present study was designed to determine the potential neuroprotective effects of chrysin, a natural flavonoid compound, against TBI-induced spatial cognitive decline and the possible mechanisms involved. Oral administration of chrysin (25, 50, or 100 mg/kg/day) was initiated in rats immediately following the induction of the diffuse TBI model using the weight-dropping Marmarou model. Spatial cognitive ability, hippocampal synaptic plasticity, blood-brain barrier (BBB) permeability, brain water content, and histological changes were assessed at scheduled time points. The animals subjected to TBI exhibited spatial cognitive decline in the Morris water maze (MWM) test, which was accompanied by inhibition of hippocampal long-term potentiation (LTP) induction at the perforant path-dentate gyrus (PP-DG) synapses. Additionally, TBI caused BBB disruption, brain edema, and neuronal loss. Interestingly, treatment with chrysin (especially in the dose of 100 mg/kg) alleviated all the above-mentioned neuropathological changes related to TBI. The results provide evidence that chrysin improves TBI-induced spatial cognitive decline, which may be partly related to the amelioration of hippocampal synaptic dysfunction, alleviation of BBB disruption, reduction of brain edema, and prevention of neuronal loss.

Topics: Animals; Brain Concussion; Brain Edema; Brain Injuries, Traumatic; Cognitive Dysfunction; Flavonoids; Hippocampus; Maze Learning; Neuroprotective Agents; Rats

Cortical and hippocampal neuronal apoptosis and neuroinflammation are associated with behavioral deficits following traumatic brain injury (TBI).. The present study was designed to investigate the potential protective effects of flavonoid chrysin against TBI-induced vestibulomotor impairment, exploratory/locomotor dysfunctions, recognition memory decline, and anxiety/depression-like behaviors, as well as the verified possible involved mechanisms.. Chrysin (25, 50, or 100 mg/kg/day; P.O.) was administered to rats immediately after diffuse TBI induction, and it was continued for 3 or 14 days. Behavioral functions were assessed by employing standard behavioral paradigms at scheduled points in time. Three days post-TBI, inflammation status was assayed in both cerebral cortex and hippocampus using ELISA kits. Moreover, apoptosis and expression of Bcl-2 family proteins were examined by TUNEL staining and immunohistochemistry, respectively.. The results indicated that treatment with chrysin improved vestibulomotor dysfunction, ameliorated recognition memory deficit, and attenuated anxiety/depression-like behaviors in the rats with TBI. Chrysin treatment also modulated inflammation status, reduced apoptotic index, and regulated Bcl-2 family proteins expression in the brains of rats with TBI.. In conclusion, the results suggest that chrysin could be beneficial for protection against TBI-associated behavioral deficits, owing to its anti-apoptotic and anti-inflammatory properties.

Topics: Animals; Anxiety; Apoptosis; Brain; Brain Injuries, Traumatic; Depression; Flavonoids; Male; Memory Disorders; Rats; Rats, Wistar; Recognition, Psychology

Oxidative stress and apoptosis have major roles in the progression of traumatic brain injury (TBI)-associated motor and cognitive deficits. The present study was aimed to elucidate the putative effects of chrysin, a natural flavonoid compound, against TBI-induced motor and cognitive dysfunctions and possible involved mechanisms.. Chrysin (25, 50 or 100 mg/kg) was orally administered to rats starting immediately following TBI induction by Marmarou's weight-drop technique and continuously for 3 or 14 days. Neurological functions, motor coordination, learning and memory performances, histological changes, cell apoptosis, expression of pro- and anti-apoptotic proteins, and oxidative status were assayed at scheduled time points after experimental TBI.. The results indicated that treatment with chrysin improved learning and memory disabilities in passive avoidance task, and ameliorated motor coordination impairment in rotarod test after TBI. These beneficial effects were accompanied by increased the concentrations of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), decreased malondialdehyde (MDA) content, prevented neuronal loss, diminished apoptotic index, elevated the expression of anti-apoptotic Bcl-2 protein, and reduced the expression of pro-apoptotic Bax protein in the cerebral cortex and hippocampus tissues.. Our findings suggest that both anti-oxidative and anti-apoptotic properties of chrysin (especially in the dose of 100 mg/kg) are possible mechanisms that improve cognitive/motor deficits and prevent neuronal cell death after TBI.

Topics: Administration, Oral; Animals; Antioxidants; Apoptosis; Brain; Brain Injuries, Traumatic; Disease Models, Animal; Flavonoids; Learning; Male; Memory Disorders; Neuroprotective Agents; Oxidative Stress; Psychomotor Performance; Rats, Wistar