Quercetin Promotes Neuronal and Behavioral Recovery by Suppressing Inflammatory Response and Apoptosis in a Rat Model of Intracerebral Hemorrhage

Zhang, Yifan; Yi, Bo; Ma, Jianhua; Zhang, Li; Zhang, Hongtian; Yi, Yang; Dai, Y Z

doi:10.1007/s11064-014-1457-1

Cited by 79 publications

(64 citation statements)

References 37 publications

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“…It is noted that mNSS was generally used to assess a combination of motor, sensory, and balance functions [23]. Neurological function was graded on a scale of 0–18 (normal score, 0; maximal deficit score, 18).…”

Section: Methodsmentioning

confidence: 99%

Effects of Estradiol on Autophagy and Nrf-2/ARE Signals after Cerebral Ischemia

Chen

Sun

et al. 2017

Cell Physiol Biochem

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Background/Aims: Estradiol (EST) reduces the risk of stroke and decreases the incidence and progression of the disease because of its neuroprotective roles in inhibiting cell death that occurs in response to a variety of neuronal stimuli such as inflammation and oxidative stress. In this study, we determined the role played by autophagy and Nrf2-ARE signal pathways in the hippocampus regions in modulating cerebral ischemia under different EST conditions. Methods: Western blot analysis and ELISA were used to determine the protein expression of autophagy and Nrf2-ARE pathways; and the levels of pro-inflammatory cytokines (PICs) and a key marker of oxidative stress. Results: Lacking of EST amplifies autophagy and attenuates Nrf2-ARE pathway in the hippocampus CA1 region. Blocking autophagy alleviates neurological deficits following cerebral ischemia with lacking of EST levels and the effects of autophagy are associated with PIC and oxidative stress. Conclusions: EST influences the protein expression of autophagy and Nrf2-ARE signaling in the brain, which is linked to the pathophysiological processes of PICs and oxidative stress. Moreover, inhibition of autophagy plays a beneficial role in modulating neurological deficits after cerebral ischemia observed under conditions of a lower level of EST.

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Section: Methodsmentioning

confidence: 99%

Effects of Estradiol on Autophagy and Nrf-2/ARE Signals after Cerebral Ischemia

Chen

Sun

et al. 2017

Cell Physiol Biochem

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“…The dose and timing of quercetin were based on previous researches. 15,17 Different set of animals were used to undertake the analyses.…”

Section: Animal Selection and Group Allocationmentioning

confidence: 99%

“…Therefore, it has been used for many diseases, such as focal cerebral ischemia 16 and intracerebral hemorrhage. 17 Previous studies have demonstrated that quercetin can reduce inflammatory lesions and exert neuroprotective effects in the hypothalamus of high-fructose-fed rats via suppressing NLRP3 inflammasome activation. 18 Recently, quercetin has been reported to exert neuroprotective effects by suppressing inflammation in SCI rats.…”

Section: Introductionmentioning

confidence: 99%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

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Study design: Randomized experimental study. Objectives: To investigate the molecular mechanisms of quercetin in spinal cord injury (SCI) rats. Setting: China. Methods: One hundred female Sprague-Dawley rats were randomly assigned into four groups: sham group, SCI group, SCI+Vehicle (Veh) group, and the SCI+Quercetin (Que) group. The influences of quercetin on proinflammatory cytokine levels, histological changes and locomotion scale were estimated. Results: SCI significantly promoted nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation and increased proinflammatory cytokine productions in the SCI group as compared with the sham group. Quercetin administration significantly decreased reactive oxygen species production, inhibited NLRP3 inflammasome activation and reduced inflammatory cytokine levels. Moreover, quercetin administration attenuated histopathology and promoted locomotion recovery. Conclusion: Quercetin can attenuate tissue damage and improve neurological function recovery, and the mechanism may be related to the inhibition of NLRP3 inflammasome activation.

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“…It is noted that mNSS was generally used to assess a combination of motor, sensory, and balance functions [9,22]. Neurological function was graded on a scale of 0-18 (normal score, 0; maximal deficit score, 18).…”

Section: Neurological Function and Brain Edemamentioning

confidence: 99%

“…The brain slices (2 mm thick) of the contralateral and ipsilateral hemispheres and cerebellum were cut. The whole brain water content was calculated from all slices [9,22]. The brain slices were weighed to obtain the wet weight immediately and dried in an oven at 100•C for 24 hrs to obtain the dry weight.…”

Section: Neurological Function and Brain Edemamentioning

confidence: 99%

Role for HIF-1α and Downstream Pathways in Regulating Neuronal Injury after Intracerebral Hemorrhage in Diabetes

Tang

Chen

et al. 2015

Cell Physiol Biochem

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This is an Open Access article licensed under the terms of the Creative Commons AttributionNonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only.Copyright © 2015 S. Karger AG, Basel Key Words Intracerebral hemorrhage • HIF-1α • VEGF • DiabetesAbstract Background/Aims: HIF-1α is accumulated in the cellular nucleus and cytoplasm under conditions of oxygen deprivation and engaged in pathophysiologic changes of homeostasis by modulating the expression of several target genes. As an endogenous signaling protein, HIF-1α contributes to in neuroprotection, erythropoiesis, and apoptosis modulation. The purpose of this study was to examine the role played by HIF-1α in regulating neurological injury evoked by intracerebral hemorrhage (ICH) through its downstream product, namely vascular endothelial growth factor (VEGF). In particular, we examined the effects of diabetic hyperglycemia on HIF-1α response in the processing of ICH. Methods: ELISA was used to measure HIF-1α and VEGF; and Western Blot analysis to examine the protein expression of VEGFR-2 and Caspase-3. Neurological Severity Score and brain water content were used to indicate neurological function and brain edema. Results: HIF-1α and VEGF were significantly increased in the brain after induction of ICH in non-diabetic control rats and diabetic rats; however, the amplified levels of HIF-1α and VEGF were attenuated in diabetic rats (P<0.05 vs. non-diabetic rats) as compared with non-diabetic rats. Also, the protein expression of VEGF receptor subtype 2 was significantly less in the brain of diabetic rats (P<0.05 vs. nondiabetic rats). Further, cerebral infusion of HIF-1 activator stabilized VEGF levels, attenuated Caspase-3 and improved neurological deficits induced by ICH and the effects are smaller in diabetic animals. Conclusion: HIF-1α activated by ICH likely plays a beneficial role via VEGF mechanisms and response of HIF-1α is largely impaired in diabetes. This has pharmacological implications to target specific HIF-1α and VEGF pathway for neuronal dysfunction and vulnerability related to ICH.

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Quercetin Promotes Neuronal and Behavioral Recovery by Suppressing Inflammatory Response and Apoptosis in a Rat Model of Intracerebral Hemorrhage

Cited by 79 publications

References 37 publications

Effects of Estradiol on Autophagy and Nrf-2/ARE Signals after Cerebral Ischemia

Effects of Estradiol on Autophagy and Nrf-2/ARE Signals after Cerebral Ischemia

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Role for HIF-1α and Downstream Pathways in Regulating Neuronal Injury after Intracerebral Hemorrhage in Diabetes

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