Neuroprotective effect of quercetin against oxidative damage and neuronal apoptosis caused by cadmium in hippocampus

Abstract

The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats.

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

“…Important Cd sources affecting human life are cigarette smoke, refined nutrients, water pipes, coffee, tea, products released by burning coal, shellfishes, fertilizers used, dyes and batteries containing Cd, and flue gases released in industrial production stages [7]. Occupational and environmental Cd exposure cause serious damages in the tissues like the placenta, kidney, liver, testis, heart, brain, and lungs [8][9][10][11][12][13][14][15]. Several investigations confirmed its transport across the placenta and accumulation in fetuses [16,17].…”

The flavonoid quercetin ameliorates Alzheimer's disease pathology and protects cognitive and emotional function in aged triple transgenic Alzheimer's disease model mice

“…These potential uses may be due to its high oxygen radical scavenging activity or its ability to inhibit xanthine oxidase and lipid peroxidation in vitro (Fiorani et al, 2010). Furthermore, quercetin reliably exerts neuroprotective effects against agent-induced toxicity (Kanter et al, 2013) and increases the resistance of neurons to oxidative stress and excitotoxicity by modulating the mechanisms of cell death (Choi et al, 2014; Liu et al, 2013a). Other studies of quercetin have shown that it produces an anti-inflammatory effect (Garcia-Mediavilla et al, 2007) by inhibiting iNOS (Martinez-Florez et al, 2005) and regulating the expression of COX-2 (Banerjee et al, 2002; de Pascual-Teresa et al, 2004), as well as an anti-proliferative effect on some types of cancer (Park et al, 2005; Russo et al, 2014), via mechanisms that activate cell senescence, apoptosis (Russo et al, 2012) and autophagy (Psahoulia et al, 2007).…”

Relationship between Wine Consumption and Alzheimer's Disease

“…It is reported that other than Aβ synthesis, quercetin also induces inhibition of formation and extension of Aβ fibrils, added to this it also stimulates and destabilizes the preformed Aβ fibrils [112,113]. The initial protein-protein interaction of Aβ40 and Aβ42which has been proved to be necessary for Aβ oligomerization, occurs with the interference of Quercetin-3-O-glucuronide [114]. Quercetin exerts neuroprotective effects against agent-induced toxicity [115] and increases the resistance of neurons to oxidative stress and excitotoxicity by modulating the mechanisms of cell death [116].…”