Quercetin protects rat cortical neurons against traumatic brain injury

Abstract

Previous studies have demonstrated that traumatic brain injury (TBI) may cause neurological deficits and neuronal cell apoptosis. Quercetin, one of the most widely distributed flavonoids, possesses anti‑inflammatory, anti‑blood coagulation, anti‑ischemic and anti‑cancer activities, and neuroprotective effects in the context of brain injury. The purpose of the present study was to investigate the neuroprotective effects of quercetin in TBI. A total of 75 rats were randomly arranged into 3 groups as follows: Sham group (Sham); TBI group (TBI); and TBI + quercetin group (Que). Brain edema was evaluated by analysis of brain water content. The neurobehavioral status of the rats was evaluated by Neurological Severity Scoring. Immunohistochemical and western blot analyses were used to measure the expression of certain proteins. The results of the present study demonstrated that post‑TBI administration of quercetin may attenuate brain edema, in addition to improving motor function in rats. Additionally, quercetin caused a marked inhibition of extracellular signal‑regulated kinase 1/2 phosphorylation and activated Akt serine/threonine protein kinase phosphorylation, which may result in attenuation of neuronal apoptosis. The present study provided novel insights into the mechanism through which quercetin may exert its neuroprotective activity in a rat model of TBI.

Brain Injury–Mediated Neuroinflammatory Response and Alzheimer’s Disease

“…Flavonoids show anti-inflammatory, anti-ischemic, anti-cancer, anti-bacterial, and anti-viral and neuroprotective characteristics. Quercetin, a flavonoid has been shown to be neuroprotective in animal models of TBI, through reducing brain edema and neuronal apoptosis with improved motor function tests (Du and others 2018). Other flavonoids such as genistein and pycnogenol also show neuroprotective effect with functional recovery in animal models of TBI.…”

“…Studies have shown that Apoε4-associated phospholipid dysregulation-mediates phosphorylation of tau after repetitive blast-induced TBI in mice. Apoε and its subset Apoε4 have been shown to be involved in Aβ toxicity, neuroinflammation, and BBB disruption (Zhao and others 2018). Chronic allergic diseases such as asthma in which mast cells are increased and heavily activated are strongly linked to phosphorylation of tau, dementia, and severity of AD (Bolós and others 2017).…”

Quercetin Limits the Progression of Oxidative and Nitrosative Stress in the Rats’ Tissues After Experimental Traumatic Brain Injury

“…The most researchers consider hypoxia and local cerebral ischemia as the leading pathogenetic mechanisms of TBI [1,4]. In these conditions, the production of reactive oxygen and nitrogen species (ROS / RNS) considerably increases that in turn triggers the activation of free radical oxidation in the cerebral tissues and further emergence of a complex of structural and functional disorders of nerve cell membranes.…”

“…Depending on the concentration and other causes, ROS / RNS can perform either a physiological role in the regulation of cerebral functions (inter-and intra-neural signaling, synaptic plasticity, cerebral hemodynamics, oscillatory activity of neurons, etc. ), or have a negative effect on the CNS functioning by causing oxidative-nitrosative stress [4].…”

Recent Trends in Potential Therapeutic Applications of the Dietary Flavonoid Didymin

“…However, the mechanism underlying the neuroprotection is not clear, but plainly relevant to the increased cerebral blood flow, reduced ischemia-related cell apoptosis, and resulted in increased neuronal viability. Dietary flavonoids could also affect the ability of human platelets to aggregate and capillary fragility, and participate in antioxidant and immune regulation mechanisms [ 13 , 14 ].…”