Neuroprotective effect of helium after neonatal hypoxic ischemia: a narrative review

KATP channels are present on the surface of cardiac internal membranes, skeletal muscle, brain, and mitochondrial membranes. KATP channels can be activated with selective drugs including diazoxide and cromakalim that may be able to limit ischemia-induced damage or brain cell death. KATP channels have no relationship with a homogenous group, while other channels do not have the same combinations. This study was to characterize the effects of the neuro-protective KATP channel openers diazoxide and cromakalim in neonatal rats with hypoxic-ischemic encephalopathy (HIE) induced by intrauterine asphyxia. Seventy-two hours-old Sprague Dawley rat pups were subjected to intrauterine asphyxia and hypoxia for 30 min, and then randomly assigned to seven groups: Vehicle, Hypoxic-ischemia (HI), Diazoxide (Dia), Cromakalim (Cro), Diazoxide+Glibenclamide (Dia + Gli), Cromakalim+Glibenclamide (Cro + Gli), and Solvent (NaOH). Brain injury was maintained by neurologic deficit or mass injury 72 hours after HI. Moreover, gene expression of KATP channels was measured by RT-PCR 72 hours after HI. Results showed that the hippocampus and cortex had the most serious injury after HI, next highest injury was in the cerebellum, and the least amount of injury was in the thalamus and brainstem. Diazoxide and cromakalim showed a neuroprotective effect to the five brain regions tested after intrauterine asphyxia. The neuroprotective effect between diazoxide and cromakalim was not statistically significant and could be inhibited by glibenclamide. Diazoxide and cromakalim had the strongest neuroprotective effect in the hippocampus and cortex, which showed the most serious injury after intrauterine asphyxia.

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The Neuroprotective Effect of Sodium Butyrate on Short-Term Memory and Serum Level of B-cell lymphoma 2 in a Rat Model of Cerebral Hypoxic-Ischemia

The Neuroscience Journal of Shefaye Khatam ◽

10.29252/shefa.6.1.34 ◽

2018 ◽

Vol 6 (1) ◽

pp. 34-40 ◽

Cited By ~ 1

Author(s):

Samira Sahraeian ◽

Mohammad Amin Edalatmanesh ◽

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Keyword(s):

Serum Level ◽

Sodium Butyrate ◽

Rat Model ◽

Short Term Memory ◽

Cell Lymphoma ◽

Neuroprotective Effect ◽

B Cell Lymphoma ◽

Short Term ◽

Term Memory ◽

Hypoxic Ischemia

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Abstract #255: Glimepiride – Bench to Bedside: Narrative Review of the Technological Advancement Update

Endocrine Practice ◽

10.1016/s1530-891x(20)44375-7 ◽

2017 ◽

Vol 23 ◽

pp. 60

Author(s):

Altamash Shaikh ◽

Anuj Maheshwari ◽

Banshi Saboo ◽

Ashok Jhingan ◽

Shriram Kulkarni ◽

...

Keyword(s):

Narrative Review ◽

Technological Advancement

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Resveratrol Reduces Matrix Metalloproteinase-2 Activity Induced by Oxygen-Glucose Deprivation and Reoxygenation in Human Cerebral Microvascular Endothelial Cells

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000119 ◽

2012 ◽

Vol 82 (4) ◽

pp. 267-274 ◽

Cited By ~ 5

Author(s):

Zahide Cavdar ◽

Mehtap Y. Egrilmez ◽

Zekiye S. Altun ◽

Nur Arslan ◽

Nilgun Yener ◽

...

Keyword(s):

Endothelial Cells ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Neurovascular Unit ◽

Glucose Deprivation ◽

Matrix Metalloproteinase 2 ◽

Microvascular Endothelial Cells ◽

Oxygen Glucose Deprivation ◽

Microvascular Endothelial

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.

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