Antioxidant Strategies in Neurocritical Care

Hanafy, Khalid A.; Selim, Magdy

doi:10.1007/s13311-011-0085-6

Cited by 21 publications

(12 citation statements)

References 128 publications

(131 reference statements)

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“…No obvious neurological deficits were observed in the Sham operation group (17 [17, 18]), though the Garcia score in the Control group (8 [7, 10]) decreased significantly when compared with the Sham group ( P < 0.05) (Fig. 1D).…”

Section: Resultsmentioning

confidence: 99%

“…Oxidative stress, which plays a vital role in the pathogenesis of cerebral I/R injury [5, 6], is caused by an imbalance between the production of ROS and its effective removal by endogenous scavenger enzymes and protective antioxidants [7]. Oxidative modification of intracellular molecules, such as proteins, lipids, and DNA, by ROS leads to neuronal injury and necrosis [8, 9].…”

Section: Introductionmentioning

confidence: 99%

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α-Lipoic Acid Promotes Neurological Recovery After Ischemic Stroke by Activating the Nrf2/HO-1 Pathway to Attenuate Oxidative Damage

Maharjan

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Alpha-lipoic acid (α-LA) has been demonstrated to be protective against cerebral ischemia injury. Herein, we investigate the neuroprotective effect and underlying mechanisms of α-LA. Methods: In vivo study, α-LA was administered intravenously upon reperfusion of transient middle cerebral artery occlusion. Garcia score was used to evaluate neurologic recovery. Infarct volume was examined by TTC staining, and oxidative damage was evaluated by ELISA assay. In an in vitro study, neurons were pretreated with α-LA at different doses and then subjected to OGD. Lentiviral vectors were applied to knockdown nuclear factor-erythroid 2-related factor-2 (Nrf2) or heme oxygenase-1 (HO-1). Cell viability was measured using CCK8. Protein expression was evaluated using western blot, and immunofluorescence staining was assessed. Results: α-LA significantly reduced the infarct volume, brain edema, and oxidative damage and promoted neurologic recovery in rats. Pretreatment of α-LA caused an obvious increase in cell viability and a decrease in intracellular reactive oxygen species. Western blot analyses and immunofluorescence staining demonstrated a distinct increase in Nrf2 and HO-1 protein expression. Conversely, knockdown of Nrf2 or HO-1 resulted in the down-regulation of HO-1 protein and inhibited the neuroprotective effect of α-LA. Conclusion: α-LA treatment is neuroprotective and promotes functional recovery after ischemic stroke by attenuating oxidative damage, which is partially mediated by the Nrf2/HO-1 pathway.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

α-Lipoic Acid Promotes Neurological Recovery After Ischemic Stroke by Activating the Nrf2/HO-1 Pathway to Attenuate Oxidative Damage

Maharjan

Wang

et al. 2017

Cell Physiol Biochem

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“…The pathological process of survival and rehabilitation in patients after ICH involves complex mechanisms [ 197 ]. Secondary brain injuries after ICH include nerve cell toxicity, microglial cell activation, cerebral vascular injury, blood brain barrier damage, arterial venous recanalization and reconstruction, and even other organ damage caused by the interaction of oxidative stress and inflammation [ 198 ]. These harmful factors must be effectively addressed to make clinically effective treatment strategies possible.…”

Section: Discussionmentioning

confidence: 99%

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Duan

Wen

Shen

et al. 2016

Oxidative Medicine and Cellular Longevity

221

177

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Hemorrhagic stroke is a common and severe neurological disorder and is associated with high rates of mortality and morbidity, especially for intracerebral hemorrhage (ICH). Increasing evidence demonstrates that oxidative stress responses participate in the pathophysiological processes of secondary brain injury (SBI) following ICH. The mechanisms involved in interoperable systems include endoplasmic reticulum (ER) stress, neuronal apoptosis and necrosis, inflammation, and autophagy. In this review, we summarized some promising advances in the field of oxidative stress and ICH, including contained animal and human investigations. We also discussed the role of oxidative stress, systemic oxidative stress responses, and some research of potential therapeutic options aimed at reducing oxidative stress to protect the neuronal function after ICH, focusing on the challenges of translation between preclinical and clinical studies, and potential post-ICH antioxidative therapeutic approaches.

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“…Since the brain is involved in most metabolic processes, it is highly exposed to OS [13,14,20] . Hence, BOLD-fMRI is a suitable imaging approach allowing spatial localization of the brain oxygenation change [8][9][10][11][12][13][14][15]21] . This technique is also used to assess BOLD phenomena that are directly linked to brain activity/plasticity and OS [7,8,13,14,[20][21][22][23][24][25][26][27][28][29] .…”

Section: Discussionmentioning

confidence: 99%

Blood Oxygenation Level-Dependent Functional MRI of Early Evidences of Brain Plasticity after Hemodialysis Session by Helixone Membrane of Patients with Indices of Adrenal Deficiency

Boujraf¹,

Belaïch²,

Housni³

et al. 2017

Ann Neurosci

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Background: Various alterations of hypothalamic-pituitary-adrenal axis function have been described in patients with chronic renal failure. Nevertheless, controversial evidences were stated about the association between adrenal function deficiency (AD) and hemodialysis (HD). Purpose: The goal of this paper was to estimate indirect indices of the adrenal gland dysfunction which is potentially influenced by oxidative stress (OS) that still generates brain plasticity and reorganization of the functional control.Methods: Two male patients undergoing HD by the synthetic Helixone membrane for more than 6 months at the HD Center of the University Hospital of Fez, Fez, Morocco, were recruited. They underwent identical assessment immediately before and after the full HD session; this consisted of a blood ionogram revealing rates of sodium and calcium, and brain blood oxygenation level-dependent functional MRI (BOLD-fMRI) using a motor paradigm in block design. Results: The blood ionogram revealed hypercalcemia and hyponatremia in both patients. Both biological assessment and BOLD-fMRI study results revealed a high level of OS that induced activation of a significantly large brain volume area suggesting the occurrence of possible brain plasticity and functional control reorganization induced by free radicals and enhanced by AD. Conclusion: The occurrence of brain plasticity and functional control reorganization was demonstrated in both patients studied who were undergoing HD by BOLD-fMRI with a notable sensitivity; this plasticity is induced by elevated OS occasioned by HD technique itself and probably amplified by AD. Similar results were found in a previous study performed on the same patients undergoing HD by a polysulfone membrane.

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Antioxidant Strategies in Neurocritical Care

Cited by 21 publications

References 128 publications

α-Lipoic Acid Promotes Neurological Recovery After Ischemic Stroke by Activating the Nrf2/HO-1 Pathway to Attenuate Oxidative Damage

α-Lipoic Acid Promotes Neurological Recovery After Ischemic Stroke by Activating the Nrf2/HO-1 Pathway to Attenuate Oxidative Damage

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Blood Oxygenation Level-Dependent Functional MRI of Early Evidences of Brain Plasticity after Hemodialysis Session by Helixone Membrane of Patients with Indices of Adrenal Deficiency

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