Neuroprotective potential of the NF-κB inhibitor peptide IKK-NBD in cerebral ischemia-reperfusion injury☆

Desai, Abhishek; Singh, Nitya; Raghubir, Ram

doi:10.1016/j.neuint.2010.09.006

Cited by 41 publications

(25 citation statements)

References 52 publications

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“…IKK-NBD, TAT-NBD, selective 5-lipoxygenase inhibitor etc. which have shown promise in preventing ischemic brain injury in different experimental systems and their efficacy should also be tested in AD animal or cell-based models [133][134][135]. It has been shown that p38 MAP kinase activity regulates transcriptional activity of NF-kB, and in AD brain p38 activity is increased [136,137].…”

Section: Inhibitors Of Nf-κb: Therapeutic Potential In Admentioning

confidence: 99%

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection

Kaur¹,

Banerjee²,

Bir³

et al. 2015

CTMC

100

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Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. The review summarizes the facts about redox-signaling cascade in the cells operating through an array of kinases, phosphatases and transcription factors and their downstream components. The biology of NF-κB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. The possibility of identifying new disease-modifying drugs for AD targeting NF-κBsignaling cascade has been discussed in the end.

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Section: Inhibitors Of Nf-κb: Therapeutic Potential In Admentioning

confidence: 99%

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection

Kaur¹,

Banerjee²,

Bir³

et al. 2015

CTMC

100

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“…Pervious experimental studies in rodents showed that inhibition of NF-KB could decreased inflammation and improve brain ischemia outcome [51,52].…”

Section: Discussionmentioning

confidence: 99%

Pre-Treatment with Metformin in Comparison with Post-Treatment Reduces Cerebral Ischemia Reperfusion Induced Injuries in Rats

Karimipour

Shojaei‐Zarghani

Milani

et al. 2018

BEAT

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Objective: To explore the effects of pre versus post ischemic treatment with metformin after global cerebral ischemia in rats. Methods: Male Wister rats underwent forebrain ischemia by bilateral common carotid artery occlusion for 17 min. Metformin (200 mg/kg) or vehicle was given orally by gavage for 7-14 days. Rats were divided into: control, metformin pre-treatment, metformin post-treatment and metformin pre and post continuous treatment groups. Cerebral infarct size, histopathology, myeloperoxidase and serum malondialdehyde were measured 7 days after ischemia. Results: Histopathological analysis showed that metformin pre-treatment significantly decreased leukocyte infiltration, myeloperoxidase activity and also malondialdehyde level. Metformin pre-treatment and metformin post-treatment reduced infarct size compared with the control group, but it was not significant in the pre and post continuous treatment group. Conclusion: Our findings suggest that pre-treatment with metformin in comparison with post-treatment in experimental stroke can reduce the extent of brain damage and is more neuroprotective at least in part by inhibiting oxidative stress and inflammation.

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“…In response to stimuli, including free radicals, which have been implicated in the pathogenesis of cerebral ischemia, IjBs are phosphorylated by the IjB kinase, and subsequently degraded, releasing NF-jB to translocate into the nucleus where it binds to a jB-specific DNA motif and regulates transcription of target genes, including immunological NOS (iNOS), which are known to be induced in cerebral ischemia and capable of mediating the deleterious effect [56,57]. Moreover, NF-jB is activated at earlier reperfusion time points and that early NF-jB inhibition in transient focal ischemia has a beneficial effect [58].…”

Section: Discussionmentioning

confidence: 99%

Preconditioning with a Novel Metallopharmaceutical NO Donor in Anesthetized Rats Subjected to Brain Ischemia/Reperfusion

et al. 2011

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Rut-bpy is a novel nitrosyl-ruthenium complex releasing NO into the vascular system. We evaluated the effect of Rut-bpy (100 mg/kg) on a rat model of brain stroke. Forty rats were assigned to four groups (Saline solution [SS], Rut-bpy, SS+ischemia-reperfusion [SS+I/R] and Rut-bpy+ischemia-reperfusion [Rut-bpy+I/R]) with their mean arterial pressure (MAP) continuously monitored. The groups were submitted (SS+I/R and Rut-bpy+I/R) or not (SS and Rut-bpy) to incomplete global brain ischemia by occlusion of the common bilateral carotid arteries during 30 min followed by reperfusion for further 60 min. Thirty minutes before ischemia, rats were treated pairwise by intraperitoneal injection of saline solution or Rut-bpy. At the end of experiments, brain was removed for triphenyltetrazolium chloride staining in order to quantify the total ischemic area. In a subset of rats, hippocampus was obtained for histopathology scoring, nitrate and nitrite measurements, immunostaining and western blotting of the nuclear factor- κB (NF-κB). Rut-bpy pre-treatment decreased MAP variations during the transition from brain ischemia to reperfusion and decreased the fractional injury area. Rut-bpy pre-treatment reduced NF-κB hippocampal immunostaining and protein expression with improved histopathology scoring as compared to the untreated operated control. In conclusion, Rut-bpy improved the total brain infarction area and hippocampal neuronal viability in part by inhibiting NF-κB signaling and helped to stabilize the blood pressure during the transition from ischemia to reperfusion.

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Neuroprotective potential of the NF-κB inhibitor peptide IKK-NBD in cerebral ischemia-reperfusion injury☆

Cited by 41 publications

References 52 publications

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection

Pre-Treatment with Metformin in Comparison with Post-Treatment Reduces Cerebral Ischemia Reperfusion Induced Injuries in Rats

Preconditioning with a Novel Metallopharmaceutical NO Donor in Anesthetized Rats Subjected to Brain Ischemia/Reperfusion

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Neuroprotective potential of the NF-κB inhibitor peptide IKK-NBD in cerebral ischemia-reperfusion injury☆

Cited by 41 publications

References 52 publications

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer&#39;s Disease: The NF-&#954;B Connection

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer&#39;s Disease: The NF-&#954;B Connection

Pre-Treatment with Metformin in Comparison with Post-Treatment Reduces Cerebral Ischemia Reperfusion Induced Injuries in Rats

Preconditioning with a Novel Metallopharmaceutical NO Donor in Anesthetized Rats Subjected to Brain Ischemia/Reperfusion

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Product

Resources

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Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection

Reactive Oxygen Species, Redox Signaling and Neuroinflammation in Alzheimer's Disease: The NF-κB Connection