scholarly journals Protective Effect of Diphenhydramine against Traumatic Brain Injury in Rats via Modulation of Oxidative Stress and Inflammation

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 47-53 ◽  
Author(s):  
Wenyong Pan ◽  
Zhigang Cao ◽  
Dongyang Liu ◽  
Yingbin Jiao
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protective Effect ◽  
Neuronal Degeneration ◽  
Neuroprotective Effect ◽  
B Cell Lymphoma ◽  
Treated Group ◽  
Dependent Manner ◽  
And Oxidative Stress

Background: Traumatic brain injury (TBI) is considered a major burden across the globe affecting both individuals and their families. Therefore, the present study was conducted to determine the protective effect of diphenhydramine (DPM) against TBI in experimental rats. Methods: The effect of DPM was evaluated on the cerebral edema (CE) and neuronal degeneration after the induction of experimental brain injury in rats. The effect of DPM was also investigated on the inflammatory cytokines, for example, tumor necrosis factor-α and interleukin 1β and oxidative stress markers, such as malondialdehyde, superoxide dismutase, and glutathione peroxidase. Western blot analysis was used to investigate the effect of DPM on B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cleaved caspase-3. Results: Results of the study suggest that DPM causes reduction in CE and prevents neuronal degeneration. It also causes reduction in inflammation and oxidative stress in a dose-dependent manner. The level of Bax was found to be elevated, together with reduction in the Bcl-2 level in the DPM-treated group. Conclusion: DPM exerts a neuroprotective effect after TBI via the attenuation of oxidative stress, inflammation, and mitochondrial apoptosis pathways.

Rhamnazin Ameliorates Traumatic Brain Injury in Mice via Reduction in Apoptosis, Oxidative Stress, and Inflammation

2021 ◽  
pp. 1-8
Author(s):  
Boxiao Yang ◽  
Rui Zhang ◽  
Qire Sa ◽  
Yanli Du
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Flow Cytometry ◽  
Brain Injury ◽  
Western Blot ◽  
Protective Effect ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Neuronal Degeneration ◽  
Flow Cytometry Analysis

<b><i>Background:</i></b> Traumatic brain injury (TBI) is posing serious health challenges for people across the globe due to high morbidity and mortality. However, none of the agents prevents or limits the damage caused by TBI because of its multifactorial etiology. Thus, the discovery of novel agents which can act via several pathways could serve the purpose and afford favorable consequence against TBI. Therefore, in the present article, we intended to investigate the protective effect of rhamnazin (RMZ), a dimethoxyflavone against experimentally induced TBI in mice. <b><i>Methods:</i></b> The effect of RMZ was investigated on cerebral edema and grip test score after induction of experimental brain injury in rats. The effect of RMZ was also investigated on neuronal degeneration in brain tissues of the experimental mice via Nissl staining and flow cytometry analysis. The expression of Bax and Bcl-2 was also quantified using Western blot analysis. The level of inflammatory cytokines (TNF-α and IL-1β) and oxidative stress markers (malondialdehyde, superoxide dismutase, and glutathione peroxidase) was also determined using enzyme-linked immunosorbent assay. <b><i>Results:</i></b> RMZ showed a significant reduction in edema and improved grip strength. It also prevented neuronal degeneration via inhibition of neuronal apoptosis as shown by flow cytometry analysis. RMZ showed an antiapoptotic effect via reduction of Bax and increased the expression of Bcl-2 in Western blot analysis. It also showed to inhibit oxidative stress and inflammation compared to the TBI group. <b><i>Conclusion:</i></b> Collectively, our study is first to demonstrate the protective effect of RMZ against experimentally induced TBI in rats.

scholarly journals Germacrone alleviates neurological deficits following traumatic brain injury by modulating neuroinflammation and oxidative stress

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sujing Zhuang ◽  
Baogui Liu ◽  
Shifeng Guo ◽  
Yanzhong Xue ◽  
Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Neuronal Apoptosis ◽  
Spatial Learning And Memory ◽  
Dependent Manner ◽  
Dose Dependent ◽  
And Oxidative Stress

Abstract Background Germacrone (GM) is a terpenoid compound which is reported to have anti-inflammatory and anti-oxidative effects. However, its role in treating traumatic brain injury (TBI) remains largely unknown. Methods Male C57BL/6 mice were divided into the following groups: control group, TBI group [controlled cortical impact (CCI) model], CCI + 5 mg/kg GM group, CCI + 10 mg/kg GM group and CCI + 20 mg/kg GM group. GM was administered via intraperitoneal injection. The neurological functions (including motor coordination, spatial learning and memory abilities) and brain edema were measured. Nissl staining was used to detect the neuronal apoptosis. Colorimetric assays and enzyme linked immunosorbent assay (ELISA) kits were used to determine the expression levels of oxidative stress markers including myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD), as well as the expressions of inflammatory markers, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). Additionally, protein levels of Nrf2 and p-p65 were detected by Western blot assay. Results GM significantly ameliorated motor dysfunction, spatial learning and memory deficits of the mice induced by TBI and it also reduced neuronal apoptosis and microglial activation in a dose-dependent manner. Besides, GM treatment reduced neuroinflammation and oxidative stress compared to those in the CCI group in a dose-dependent manner. Furthermore, GM up-regulated the expression of antioxidant protein Nrf2 and inhibited the expression of inflammatory response protein p-p65. Conclusions GM is a promising drug to improve the functional recovery after TBI via repressing neuroinflammation and oxidative stress.

Minocycline effects on cerebral edema: Relations with inflammatory and oxidative stress markers following traumatic brain injury in mice

2009 ◽  
Vol 1291 ◽  
pp. 122-132 ◽  
Author(s):  
Shadi Homsi ◽  
Fabiola Federico ◽  
Nicole Croci ◽  
Bruno Palmier ◽  
Michel Plotkine ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Edema ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
And Oxidative Stress

scholarly journals Traumatic Brain Injury: Oxidative Stress and Novel Anti-Oxidants Such as Mitoquinone and Edaravone

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 943 ◽  
Author(s):  
Helene Ismail ◽  
Zaynab Shakkour ◽  
Maha Tabet ◽  
Samar Abdelhady ◽  
Abir Kobaisi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuroprotective Effect ◽  
Treatment Options ◽  
Free Radical Scavenger ◽  
Health Concern ◽  
Radical Scavenger ◽  
History Of ◽  
Ionic Imbalance

Traumatic brain injury (TBI) is a major health concern worldwide and is classified based on severity into mild, moderate, and severe. The mechanical injury in TBI leads to a metabolic and ionic imbalance, which eventually leads to excessive production of reactive oxygen species (ROS) and a state of oxidative stress. To date, no drug has been approved by the food and drug administration (FDA) for the treatment of TBI. Nevertheless, it is thought that targeting the pathology mechanisms would alleviate the consequences of TBI. For that purpose, antioxidants have been considered as treatment options in TBI and were shown to have a neuroprotective effect. In this review, we will discuss oxidative stress in TBI, the history of antioxidant utilization in the treatment of TBI, and we will focus on two novel antioxidants, mitoquinone (MitoQ) and edaravone. MitoQ can cross the blood brain barrier and cellular membranes to accumulate in the mitochondria and is thought to activate the Nrf2/ARE pathway leading to an increase in the expression of antioxidant enzymes. Edaravone is a free radical scavenger that leads to the mitigation of damage resulting from oxidative stress with a possible association to the activation of the Nrf2/ARE pathway as well.

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 Treadmill Exercise Protects Against Pentylenetetrazol-Induced Seizures and Oxidative Stress after Traumatic Brain Injury

2013 ◽  
Vol 30 (14) ◽  
pp. 1278-1287 ◽  
Author(s):  
Luiz Fernando Almeida Silva ◽  
Maurício Scopel Hoffmann ◽  
Rogério da Rosa Gerbatin ◽  
Fernando da Silva Fiorin ◽  
Fernando Dobrachinski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Treadmill Exercise ◽  
And Oxidative Stress

scholarly journals Protective effect of vitamin E on oxidative stress and sperm apoptosis in diabetic Mice

2019 ◽  
Vol 17 (2) ◽  
pp. 127 ◽  
Author(s):  
Khadijeh Mirzaei Khorramabadi ◽  
Ali Reza Talebi ◽  
Abolghasem Abbasi Sarcheshmeh ◽  
Aghdas Mirjalili
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Protective Effect ◽  
Sperm Morphology ◽  
Sperm Count ◽  
Treated Group ◽  
Control Group ◽  
Diabetic Mice ◽  
And Oxidative Stress ◽  
Sperm Movement

Background: Generation of free radicals and oxidative stress are a major contributorto diabetes. These factors lead to the development of diabetic testicles disorders.Objective: In this study, the protective effect of vitamin E on functional disordersassociated with diabetes induced oxidative stress in male reproductive systems hasbeen investigated.Materials and Methods: Thirty-three adult male Mice were divided into control,diabetic, and untreated diabetic groups. Streptozotocin was used to induce diabetes.In the treated group, vitamin E was given to the Mice intraperitoneally for 30 days.Then, animals were anesthetized and sacrificed. Animal testicles were isolated andhomogenized in phosphate buffer and used for measuring sperm count, motility andsurvival of sperm, MDA concentration and antioxidant capacity (TAC). Apoptosis wasalso performed with the TUNEL test.Results: The results of reduction (12.03±98.11) TAC, MDA concentration (–28.5±2.58),sperm motility (unstable sperma= 86.4±7.48), sperm count (171.51), Sperm morphology(natural morphology= 49.69±31.93) and abnormal morphology (9.77±49.7)with increased oxidative damage. These changes were statistically significant incomparison with the control group for all variables other than MDA (p= 0.05). Treatmentof vitamin E diabetic Mice improved the ability of antioxidants to prevent oxidativedamage in the testicles, restore the sperm movement, and increase the number ofnormal sperm as well as TAC. The level of apoptosis in the treated group has decreasedcompared to the untreated group.Conclusion: Vitamin E protects the reproductive system against diabetes mellitus.Therefore, it was concluded that vitamin E may be a suitable agent for protecting thesperm and testicular parameters against undesirable effects of diabetes.

scholarly journals Apelin-13/APJ system attenuates early brain injury via suppression of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation and oxidative stress in a AMPK-dependent manner after subarachnoid hemorrhage in rats

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Weilin Xu ◽  
Tao Li ◽  
Liansheng Gao ◽  
Jingwei Zheng ◽  
Jun Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Er Stress ◽  
Early Brain Injury ◽  
Inflammasome Activation ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
And Oxidative Stress

Abstract Background Neuroinflammation and oxidative stress play important roles in early brain injury following subarachnoid hemorrhage (SAH). This study is the first to show that activation of apelin receptor (APJ) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-associated inflammation and oxidative stress after SAH. Methods Apelin-13, apelin siRNA, APJ siRNA, and adenosine monophosphate-activated protein kinase (AMPK) inhibitor-dorsomorphin were used to investigate if the activation of APJ could provide neuroprotective effects after SAH. Brain water content, neurological functions, blood-brain barrier (BBB) integrity, and inflammatory molecules were evaluated at 24 h after SAH. Western blotting and immunofluorescence staining were applied to assess the expression of target proteins. Results The results showed that endogenous apelin, APJ, and p-AMPK levels were significantly increased and peaked in the brain 24 h after SAH. In addition, administration of exogenous apelin-13 significantly alleviated neurological functions, attenuated brain edema, preserved BBB integrity, and also improved long-term spatial learning and memory abilities after SAH. The underlying mechanism of the neuroprotective effects of apelin-13 is that it suppresses microglia activation, prevents ER stress from overactivation, and reduces the levels of thioredoxin-interacting protein (TXNIP), NOD-like receptor pyrin domain-containing 3 protein (NLRP3), Bip, cleaved caspase-1, IL-1β, TNFα, myeloperoxidase (MPO), and reactive oxygen species (ROS). Furthermore, the use of APJ siRNA and dorsomorphin abolished the neuroprotective effects of apelin-13 on neuroinflammation and oxidative stress. Conclusions Exogenous apelin-13 binding to APJ attenuates early brain injury by reducing ER stress-mediated oxidative stress and neuroinflammation, which is at least partly mediated by the AMPK/TXNIP/NLRP3 signaling pathway.

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