Neuroprotective effects of various doses of topiramate against methylphenidate-induced oxidative stress and inflammation in isolated rat amygdala: the possible role of CREB/BDNF signaling pathway

Marine habitats offer a rich reservoir of new bioactive compounds with great pharmaceutical potential; the variety of these molecules is unique, and its production is favored by the chemical and physical conditions of the sea. It is known that marine organisms can synthesize bioactive molecules to survive from atypical environmental conditions, such as oxidative stress, photodynamic damage, and extreme temperature. Recent evidence proposed a beneficial role of these compounds for human health. In particular, xanthines, bryostatin, and 11-dehydrosinulariolide displayed encouraging neuroprotective effects in neurodegenerative disorders. This review will focus on the most promising marine drugs’ neuroprotective potential for neurodegenerative disorders, such as Parkinson’s and Alzheimer’s diseases. We will describe these marine compounds’ potential as adjuvant therapies for neurodegenerative diseases, based on their antioxidant, anti-inflammatory, and anti-apoptotic properties.

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Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽

10.3390/molecules26144138 ◽

2021 ◽

Vol 26 (14) ◽

pp. 4138

Author(s):

Yeon-Jin Cho ◽

Sun-Hye Choi ◽

Ra-Mi Lee ◽

Han-Sung Cho ◽

Hyewhon Rhim ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Signaling Pathway ◽

Reactive Oxygen ◽

Akt Signaling ◽

Atp Depletion ◽

Oxygen Species ◽

Akt Signaling Pathway ◽

Neuroprotective Effects ◽

Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

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Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/6801587 ◽

2020 ◽

Vol 2020 ◽

pp. 1-20

Author(s):

Xiao Hu ◽

Shirong Li ◽

Desislava Met Doycheva ◽

Lei Huang ◽

Cameron Lenahan ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Rat Model ◽

Neuronal Apoptosis ◽

Neuronal Degeneration ◽

Infarct Volume ◽

Neurological Deficits ◽

Tunel Staining ◽

Artery Ligation ◽

Neuroprotective Effects

Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.

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Prominence of Oxidative Stress in the Management of Anti-tuberculosis Drugs Related Hepatotoxicity

Drug Metabolism Letters ◽

10.2174/1872312813666190716155930 ◽

2020 ◽

Vol 13 (2) ◽

pp. 95-101 ◽

Cited By ~ 1

Author(s):

Preena John ◽

Pravin P. Kale

Keyword(s):

Oxidative Stress ◽

Membrane Permeability ◽

Signaling Pathway ◽

Critical Condition ◽

Permeability Transition ◽

Review Article ◽

Present Review ◽

Membrane Permeability Transition ◽

Hepatic Glutathione

: Advanced medical services and treatments are available for treating Tuberculosis. Related prevalence has increased in recent times. Unfortunately, the continuous consumption of related drugs is also known for inducing hepatotoxicity which is a critical condition and cannot be overlooked. The present review article has focused on the pathways causing these toxicities and also the role of enzyme CYP2E1, hepatic glutathione, Nrf2-ARE signaling pathway, and Membrane Permeability Transition as possible targets which may help in preventing the hepatotoxicity induced by the drugs used in the treatment of tuberculosis.

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Edaravone attenuates oxidative stress induced by chronic cerebral hypoperfusion injury: role of ERK/Nrf2/HO-1 signaling pathway

Neurological Research ◽

10.1080/01616412.2017.1376457 ◽

2017 ◽

Vol 40 (1) ◽

pp. 1-10 ◽

Cited By ~ 23

Author(s):

Dandan Zhang ◽

Yining Xiao ◽

Peiyuan Lv ◽

Zhenjie Teng ◽

Yanhong Dong ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Chronic Cerebral Hypoperfusion ◽

Cerebral Hypoperfusion

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Modulation ofN-methyl-d-aspartate receptors in isolated rat heart

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2017-0056 ◽

2017 ◽

Vol 95 (11) ◽

pp. 1327-1334 ◽

Cited By ~ 5

Author(s):

Ivan Srejovic ◽

Vladimir Zivkovic ◽

Tamara Nikolic ◽

Nevena Jeremic ◽

Isidora Stojic ◽

...

Keyword(s):

Oxidative Stress ◽

Rat Heart ◽

Isolated Rat Heart ◽

Albino Rats ◽

Oxidative Stress Biomarkers ◽

Stress Biomarkers ◽

Combined Application ◽

Wistar Albino Rats ◽

Isolated Rat

Considering the limited data on the role of NMDA-Rs in the cardiovascular system, the aim of the present study was to examine the effects of NMDA and DL-Hcy TLHC, alone and in combination with glycine, memantine, and ifenprodil, in the isolated rat heart. The hearts of Wistar albino rats were retrogradely perfused according to the Langendorff technique at a constant perfusion pressure. The experimental protocol for all experimental groups included the stabilization period, application of estimated substance for 5 min, followed by a washout period of 10 min. Using a sensor placed in the left ventricle, we registered the following parameters of myocardial function: dp/dtmax, dp/dtmin, SLVP, DVLP, HR; CF was measured using flowmetry). We estimated the following oxidative stress biomarkers in the coronary venous effluent using spectrophotometry: TBARS, NO2−, O2−, and H2O2. NMDA alone did not induce any change in any of the observed parameters, while DL-Hcy TLHC alone, as well as a combined application of NMDA and DL-Hcy TLHC with glycine, induced a reduction of most cardiodynamic parameters. Memantine and ifenprodil induced a reduction of cardiodynamic parameters and CF, as well as some oxidative stress biomarkers.

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EGCG Promotes Neurite Outgrowth through the Integrin β1/FAK/p38 Signaling Pathway after Subarachnoid Hemorrhage

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/8810414 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Yuyuan Zhang ◽

Mengguo Han ◽

Xiaoxue Sun ◽

Guojun Gao ◽

Guoying Yu ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Neurite Outgrowth ◽

Signaling Pathway ◽

Cell Injury ◽

Integrin Β1 ◽

Neuroprotective Effects ◽

Neurological Score ◽

Biological Component ◽

Abnormal Neurites

The abnormal neurites have long been regarded as the main player contributing to the poor outcome of patients with subarachnoid hemorrhage (SAH). (-)-Eigallocatechin-3-gallate (EGCG), the major biological component of tea catechin, exhibited strong neuroprotective effects against central nervous system diseases; however, the role of EGCG-mediated neurite outgrowth after SAH has not been delineated. Here, the effect of reactive oxygen species (ROS)/integrin β1/FAK/p38 pathway on neurite outgrowth was investigated. As expected, oxyhemoglobin- (OxyHb-) induced excessive ROS level was significantly reduced by EGCG as well as antioxidant N-acetyl-l-cysteine (NAC). Consequently, the expression of integrin β1 was significantly inhibited by EGCG and NAC. Meanwhile, EGCG significantly inhibited the overexpression of phosphorylated FAK and p38 to basal level after SAH. As a result, the abnormal neurites and cell injury were rescued by EGCG, which eventually increased energy generation and neurological score after SAH. These results suggested that EGCG promoted neurite outgrowth after SAH by inhibition of ROS/integrin β1/FAK/p38 signaling pathway. Therefore, EGCG might be a new pharmacological agent that targets neurite outgrowth in SAH therapy.

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