Quercetin Reduces Ischemic Brain Injury by Preventing Ischemia-induced Decreases in the Neuronal Calcium Sensor Protein Hippocalcin

Park, Dong-Ju; Jeon, Seong-Jun; Kang, Ju-Bin; Koh, Phil-Ok

doi:10.1016/j.neuroscience.2020.01.015

Cited by 23 publications

(28 citation statements)

References 38 publications

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“…This finding supports the anti-oxidant potential of quercetin. Similarly, quercetin treatment attenuated the increase of caspase 3 in ischemic brain injury in rats [46,47] and Bcl2 in lipopolysaccharide-treated mice [48].…”

Section: Discussionmentioning

confidence: 86%

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats

Dora

Taha

Lebda

et al. 2021

IJMS

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Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups; the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards.

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Section: Discussionmentioning

confidence: 86%

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats

Dora

Taha

Lebda

et al. 2021

IJMS

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“…TNF-α, IL-1β, LDH, ERK, akt, EGF, MMP-9, Claudin-5, ZO-1, β-catenin, GSK-3β, Axin, LEF1, MDA, SOD, CAT, caspase-3, Bcl-2, Nrf2, NOX4, IκBα, p65 (Dai et al, 2018;Jin et al, 2019;Park et al, 2020; Calycosin 5-30 mg/kg BDNF/TrkB, TNF-α, Bcl-2, NBR1, p62, caveolin-1, claudin-5, NO, ZO-1, MMP-2, MMP-9, ROS, ER-α, RASD1, Bcl-2, SIRT1, FOXO1, Bcl-2, bax, PGC-1α (Guo et al, 2012;Hsu et al, 2020;Wang, Y et al, 2014;Wang, Y. et al, 2018) Alkaloid Berberine 0.002-100 mg/kg (in vivo), 0.5 μg/ml (in vitro)…”

Section: Discussionmentioning

confidence: 99%

“…Calcium acts as a second messenger that mediates physiologic functions. It's reported that quercetin exerted a preventative effect through attenuation of intracellular calcium overload and restoration of down-regulated hippocalcin expression during ischemic injury (Park et al, 2020). Moreover, quercetin alleviated the increasement of protein tyrosine and serine/threonine phosphatase activity, along with the reduction of ERK and Akt phosphorylation in cerebral I/R injury .…”

Section: Quercetinmentioning

confidence: 95%

Neuroprotective Effect for Cerebral Ischemia by Natural Products: A Review

Xie

et al. 2021

Front. Pharmacol.

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Natural products have a significant role in the prevention of disease and boosting of health in humans and animals. Stroke is a disease with high prevalence and incidence, the pathogenesis is a complex cascade reaction. In recent years, it’s reported that a vast number of natural products have demonstrated beneficial effects on stroke worldwide. Natural products have been discovered to modulate activities with multiple targets and signaling pathways to exert neuroprotection via direct or indirect effects on enzymes, such as kinases, regulatory receptors, and proteins. This review provides a comprehensive summary of the established pharmacological effects and multiple target mechanisms of natural products for cerebral ischemic injury in vitro and in vivo preclinical models, and their potential neuro-therapeutic applications. In addition, the biological activity of natural products is closely related to their structure, and the structure-activity relationship of most natural products in neuroprotection is lacking, which should be further explored in future. Overall, we stress on natural products for their role in neuroprotection, and this wide band of pharmacological or biological activities has made them suitable candidates for the treatment of stroke.

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“…In contrast, quercetin has been reported to inhibit mitochondria-dependent apoptotic events, cytochrome-c release, and thus prevent vascular calcification by inhibiting oxidant damage [24]. Park et al had investigated quercetin against ischemic brain injury and demonstrated that ischemia-induced glutamate and caspase-3 increases were effectively suppressed [25]. Examining the effects of quercetin supplementation against aging caused by D-galactose in the pancreatic and kidney tissues, El-Far and colleagues reported that this substance may be effective in preventing aging-related oxidant damage and suppress apoptotic and inflammatory events [26].…”

Section: Discussionmentioning

confidence: 99%

Protective effects of quercetin against cisplatin induced urogenital organ toxicity

Şener¹,

Cadirci²,

Çevik³

et al. 2020

jrp

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Cisplatin is a chemotherapeutic agent that is the first to enter treatment from organic platinum-derived drugs. Nephrotoxicity and cytotoxicity are major factors that limit its use. The aim of the study is to investigate the possible protective effects of quercetin against cisplatin-induced urogenital organ toxicity. In our study, Sprague Dawley four month old male rats were divided into 4 groups; control + saline (SF), control + quercetin (20 mg/kg for 21 days), cisplatin (7 mg/kg as a single dose) + SF and cisplatin + quercetin groups. After decapitation, the kidney, bladder, testis and corpus cavernosum tissue samples were taken to analyze caspase-3, an index of apoptosis, and oxidative stress parameters such as malondialdehyde (MDA), gluta-thione (GSH), and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Furthermore, tissues were also examined histologically. Cisplatin caused significant increases in MDA and 8-OHdG levels, demonstrating increases in lipid peroxidation and oxidative DNA damage, respectively, in all tissues. In parallel with the oxidant stress increase, the endogenous strong antioxidant GSH levels were decreased. Caspase activity and caspase 3 expressions, which we measured as an indicator of apoptosis, increased significantly with cisplatin treatment. On the other hand, treatment with quercetin, a powerful antioxidant flavonoid, reversed these changes. Histological findings also demonstrated well-preserved tissues due to quercetin treatment. In conclusion, our results suggested that quercetin, when given with cisplatin, can be protective against the chemotherapeutic induced toxicity and thus provide therapeutic benefit.

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Quercetin Reduces Ischemic Brain Injury by Preventing Ischemia-induced Decreases in the Neuronal Calcium Sensor Protein Hippocalcin

Cited by 23 publications

References 38 publications

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats

Neuroprotective Effect for Cerebral Ischemia by Natural Products: A Review

Protective effects of quercetin against cisplatin induced urogenital organ toxicity

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