IL‐1β increases necrotic neuronal cell death in the developing rat hippocampus after status epilepticus by activating type I IL‐1 receptor (IL‐1RI)

2014 ◽  
Vol 38 (1) ◽  
pp. 232-240 ◽  
Author(s):  
Jesús‐Servando Medel‐Matus ◽  
Dulce‐Mariely Álvarez‐Croda ◽  
Joel Martínez‐Quiroz ◽  
Luis Beltrán‐Parrazal ◽  
Consuelo Morgado‐Valle ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Hippocampus ◽  
Type I ◽  
Developing Rat

scholarly journals Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

2016 ◽  
Vol 88 (suppl 1) ◽  
pp. 653-663 ◽  
Author(s):  
Dulce-Mariely Álvarez-Croda ◽  
Juan Santiago-García ◽  
Jesús S. Medel-Matus ◽  
Joel Martínez-Quiroz ◽  
Angel A. Puig-Lagunes ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Mrna Expression ◽  
Dorsal Hippocampus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Control Group ◽  
Rat Pups ◽  
Fluoro Jade B ◽  
Developing Rat

The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteen-days-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohistochemical procedures; Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. IL-1β mRNA expression was increased 6 h following SE, but not at 24 h; however IL-1RI mRNA expression was unaffected when comparing with the control group. IL-1β and IL-1RI immunoreactivity was not detected in control animals. IL-1β and IL-1RI were expressed in the CA1 pyramidal layer, the dentate gyrus granular layer and the hilus 6 h after SE, whereas injured cells were detected 24 h following seizures. Early expression of IL-1β and IL-1RI in the hippocampus could be associated with SE-induced neuronal cell death mechanisms in the developing rat.

scholarly journals Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1702
Author(s):  
Sereen Sandouka ◽  
Tawfeeq Shekh-Ahmad
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Antioxidant Capacity ◽  
Temporal Lobe ◽  
Epileptiform Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

scholarly journals Protective Effects of Bupivacaine against Kainic Acid-Induced Seizure and Neuronal Cell Death in the Rat Hippocampus

2015 ◽  
Vol 38 (4) ◽  
pp. 522-530 ◽  
Author(s):  
Kuan Ming Chiu ◽  
Chia Chan Wu ◽  
Ming Jiuh Wang ◽  
Ming Yi Lee ◽  
Su Jane Wang
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Hippocampus ◽  
Protective Effects

1208 Increase in fibrinolytic activity and neuronal cell death by kainic acid injection in rat hippocampus

1997 ◽  
Vol 28 ◽  
pp. S150
Author(s):  
Nagai Nobuo ◽  
Endo Akira ◽  
Takahashi Hirosi ◽  
Ihara Hayato ◽  
Urano Tetsumei ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Fibrinolytic Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Hippocampus ◽  
Acid Injection ◽  
Kainic Acid Injection
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