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

2017 ◽  
Vol 41 (5) ◽  
pp. 2027-2036 ◽  
Author(s):  
Litao Li ◽  
Jinghong Chen ◽  
Sujuan Sun ◽  
Jingru Zhao ◽  
Xiaoli Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Neurological Deficits ◽  
Signal Pathways ◽  
Ca1 Region ◽  
The Brain ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

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.

scholarly journals Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020 ◽  
Vol 21 (7) ◽  
pp. 2501 ◽  
Author(s):  
Thomas Nury ◽  
Gérard Lizard ◽  
Anne Vejux
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
The Body ◽  
Protein Accumulation ◽  
Common Features ◽  
Apoptosis And Inflammation ◽  
The Brain ◽  
And Oxidative Stress

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

scholarly journals Lack of mitochondrial ferritin aggravated neurological deficits via enhancing oxidative stress in a traumatic brain injury murine model

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Ligang Wang ◽  
Libo Wang ◽  
Zhibo Dai ◽  
Pei Wu ◽  
Huaizhang Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Knockout Mice ◽  
Brain Injuries ◽  
Brain Infarction ◽  
Neurological Deficits ◽  
Important Correlation ◽  
The Brain ◽  
And Oxidative Stress

Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI.

scholarly journals Energy Drink Administration in Combination with Alcohol Causes an Inflammatory Response and Oxidative Stress in the Hippocampus and Temporal Cortex of Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Alfonso Díaz ◽  
Samuel Treviño ◽  
Jorge Guevara ◽  
Guadalupe Muñoz-Arenas ◽  
Eduardo Brambila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Inflammatory Response ◽  
Temporal Cortex ◽  
Energy Drink ◽  
Brain Regions ◽  
Adult Rats ◽  
Mechanisms Of Toxicity ◽  
The Brain ◽  
And Oxidative Stress

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.

scholarly journals Buyang Huanwu Decoction Promotes Angiogenesis after Cerebral Ischemia by Inhibiting the Nox4/ROS Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Jian Shen ◽  
Kaiyuan Huang ◽  
Yu Zhu ◽  
Kangli Xu ◽  
Renya Zhan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Cell Viability ◽  
Tube Formation ◽  
Neurological Function ◽  
Neurological Deficits ◽  
Ros Generation ◽  
Buyang Huanwu Decoction ◽  
Intracellular Ros

Background. Buyang Huanwu decoction (BYHWD), an important traditional Chinese medicine (TCM), has been used clinically for centuries for the treatment of various diseases. The study aims to explore the BYHWD effects on angiogenesis and neuroprotection after cerebral ischemia/reperfusion (CI/R) injury in rats and to explore the underlying angiogenic roles and mechanisms of BYHWD in hydrogen peroxide (H2O2) induced oxidative stress in human umbilical vein endothelial cells (HUVECs) model. Methods. The effects of BYHWD on neurological function were screened by measuring neurological deficits, spatial memory function, and angiogenesis (by microvascular density (MVD) and cerebral blood flow (CBF)) after CI/R injury in middle cerebral artery occlusion (MCAO) in vivo in rats. In vitro, we examined the angiogenic roles and mechanisms of action of BYHWD in an H2O2-induced oxidative stress HUVECs model by measuring cell viability, apoptosis, vascular tube formation, intracellular ROS generation, NADPH oxidase (Nox) activity, and Nox4 protein expression. Results. BYHWD significantly improved neurological function, including neurological deficits and spatial learning and memory, and significantly increased MVD and CBF in the ischemic penumbra after CI/R injury in rats. BYHWD significantly increased cell viability, inhibited apoptosis, induced vascular tube formation, decreased intracellular ROS generation, and reduced Nox activity and Nox4 protein expression in H2O2-treated HUVECs in a dose-dependent manner. Conclusions. Our study demonstrates that BYHWD promotes neurological function recovery and increases angiogenesis. BYHWD exerts angiogenic effects against cerebral ischemic injury through the downregulation of Nox4, which results in the reduction of ROS generation.

scholarly journals Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Feng Liang ◽  
Xin Fu ◽  
Yunpengfei Li ◽  
Fanglei Han
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Protein Expression ◽  
Protective Effect ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Neuronal Injury ◽  
Cyclin B1 ◽  
The Brain ◽  
And Oxidative Stress

Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.

Dietary genistein and equol (4′, 7 isoflavandiol) reduce oxidative stress and protect rats against focal cerebral ischemia

2010 ◽  
Vol 299 (3) ◽  
pp. R871-R877 ◽  
Author(s):  
Yulin Ma ◽  
Jennifer C. Sullivan ◽  
Derek A. Schreihofer
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Hormone Replacement ◽  
Cerebral Injury ◽  
Female Rats ◽  
Neurological Deficits ◽  
Soy Isoflavone ◽  
Transient Focal Cerebral Ischemia ◽  
The Brain

High soy diets reduce injury in rat models of focal cerebral ischemia and are proposed as alternatives to hormone replacement therapy for postmenopausal women. The present study tests the hypothesis that the major soy isoflavone genistein and the daidzein metabolite equol are neuroprotective in transient focal cerebral ischemia in male and ovariectomized (OVX) female rats by inhibiting oxidative stress. Genistein is the primary circulating soy isoflavone in humans, whereas equol is the primary circulating isoflavone in rats. Male and OVX female Sprague-Dawley rats were fed an isoflavone-reduced diet alone or supplemented with genistein (500 ppm) or equol (250 ppm) for 2 wk prior to 90-min transient middle cerebral artery occlusion followed by reperfusion under isoflurane anesthesia. Indices of oxidative stress were determined 24 h after reperfusion, and cerebral injury was evaluated 3 days after reperfusion. Genistein and equol significantly reduced infarct size in both sexes. Further studies in OVX female rats revealed that this neuroprotection was accompanied by a decrease in NAD(P)H oxidase activity and superoxide levels in the brain. In addition, equol reduced plasma thiobarbituric acid reactive substances, and neurological deficits up to 7 days after injury. There were no significant differences in cerebral blood flow among treatment groups. In conclusion, dietary soy isoflavones are neuroprotective in transient focal cerebral ischemia in male and OVX female rats. These isoflavones may protect the brain via increases in endogenous antioxidant mechanisms and reduced oxidative stress.

The antioxidant Rutin counteracts the pathological impact of α-synuclein on the enteric nervous system in vitro

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Anne Christmann ◽  
Manuela Gries ◽  
Patrik Scholz ◽  
Pascal L. Stahr ◽  
Jessica Ka Yan Law ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Dopaminergic Neurons ◽  
Synaptic Vesicles ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
The Brain ◽  
And Oxidative Stress

Abstract Motoric disturbances in Parkinson’s disease (PD) derive from the loss of dopaminergic neurons in the substantia nigra. Intestinal dysfunctions often appear long before manifestation of neuronal symptoms, suggesting a strong correlation between gut and brain in PD. Oxidative stress is a key player in neurodegeneration causing neuronal cell death. Using natural antioxidative flavonoids like Rutin, might provide intervening strategies to improve PD pathogenesis. To explore the potential effects of micro (mRutin) compared to nano Rutin (nRutin) upon the brain and the gut during PD, its neuroprotective effects were assessed using an in vitro PD model. Our results demonstrated that Rutin inhibited the neurotoxicity induced by A53T α-synuclein (Syn) administration by decreasing oxidized lipids and increasing cell viability in both, mesencephalic and enteric cells. For enteric cells, neurite outgrowth, number of synaptic vesicles, and tyrosine hydroxylase positive cells were significantly reduced when treated with Syn. This could be reversed by the addition of Rutin. nRutin revealed a more pronounced result in all experiments. In conclusion, our study shows that Rutin, especially the nanocrystals, are promising natural compounds to protect neurons from cell death and oxidative stress during PD. Early intake of Rutin may provide a realizable option to prevent or slow PD pathogenesis.

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