Withanolide-A treatment exerts a neuroprotective effect via inhibiting neuroinflammation in the hippocampus after pilocarpine-induced status epilepticus

2020 ◽  
Vol 165 ◽  
pp. 106394
Author(s):  
Jing Zhu ◽  
Soojin Park ◽  
Kyoung Hoon Jeong ◽  
Won-Joo Kim
Keyword(s):  
Status Epilepticus ◽  
Neuroprotective Effect ◽  
Withanolide A

scholarly journals Neuroprotective effect of pyruvate and oxaloacetate during pilocarpine induced status epilepticus in rats

2011 ◽  
Vol 58 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Andrezza Sossai Rodrigues Carvalho ◽  
Laila Brito Torres ◽  
Daniele Suzete Persike ◽  
Maria José Silva Fernandes ◽  
Debora Amado ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Neuroprotective Effect

scholarly journals Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway

2019 ◽  
Vol 20 (4) ◽  
pp. 998 ◽  
Author(s):  
Yao-Chung Chuang ◽  
Shang-Der Chen ◽  
Chung-Yao Hsu ◽  
Shu-Fang Chen ◽  
Nai-Ching Chen ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Prolonged Seizure

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

scholarly journals The Neuroprotective Effect of Astaxanthin on Pilocarpine-Induced Status Epilepticus in Rats

2019 ◽  
Vol 13 ◽  
Author(s):  
Xiaolin Deng ◽  
Ming Wang ◽  
Sihui Hu ◽  
Yonghao Feng ◽  
Yiye Shao ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Neuroprotective Effect

Neuroprotective Effect of Felbamate After Kainic Acid-Induced Status Epilepticus

Epilepsia ◽  
1993 ◽  
Vol 34 (2) ◽  
pp. 359-366 ◽  
Author(s):  
Antonia Chronopoulos ◽  
Carl Stafstrom ◽  
Sam Thurber ◽  
Pamela Hyde ◽  
Mohamad Mikati ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Kainic Acid ◽  
Neuroprotective Effect

scholarly journals Neuroprotective effect of lithium after pilocarpine-induced status epilepticus in mice

2017 ◽  
Vol 21 (1) ◽  
pp. 125 ◽  
Author(s):  
Namgue Hong ◽  
Yun-Sik Choi ◽  
Seong Yun Kim ◽  
Hee Jung Kim
Keyword(s):  
Status Epilepticus ◽  
Neuroprotective Effect

scholarly journals TRPV1 Contributes to the Neuroprotective Effect of Dexmedetomidine in Pilocarpine-Induced Status Epilepticus Juvenile Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Xingqin Tan ◽  
Yong Zeng ◽  
Zhenzhen Tu ◽  
Pan Li ◽  
Hengsheng Chen ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Status Epilepticus ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Juvenile Rats ◽  
Transmission Electron ◽  
Mitochondrial Membrane Potential Loss

To investigate the antiepileptic and neuroprotective effects of dexmedetomidine (Dex) in pilocarpine- (Pilo-) induced status epilepticus (SE) juvenile rats, rats were randomly assigned to the following six groups (n=20): normal, normal+Dex, SE, SE+Cap, SE+Dex, and SE+Dex+Cap. The rats were treated with either diazepam (i.p., an antiepileptic drug) or Dex after the onset of SE. The Morris water maze was used to assess rat cognitive behavior. Flow cytometry was used to detect the concentrations of Ca2+, mitochondrial membrane potential, and reactive oxygen species. Transmission electron microscopy was performed to evaluate specimens of brain tissue. The levels of caspase 3 and TRPV1 were examined by western blot and immunohistochemistry (IHC). Treatment with Dex significantly decreased the escape latency of the SE rats (P<0.05). Capsaicin, a TRPV1 agonist, delivery aggravated the performance of SE rats. Pathological changes in SE rat were attenuated by Dex and deteriorated by capsaicin. Swollen mitochondria and abnormal endoplasmic reticulum were found in SE rats and were then aggravated by capsaicin and reversed by Dex. Moreover, our data showed that Dex significantly restrained calcium overload, ROS production, and mitochondrial membrane potential loss, all of which were induced by Pilo and capsaicin (P<0.05). Dex decreased the apoptotic rate in the Model SE group (P<0.05) and TRPV1 and caspase 3 expression in the Dex treatment group (P<0.05). Interestingly, all these effects of Dex were partially counteracted by the TRPV1 agonist, capsaicin (P<0.05). Our study showed that Dex exerted a neuroprotective effect in Pilo-induced SE rats by inhibiting TRPV1 expression and provided information for therapy to SE patients.

scholarly journals The Neuroprotective Effect of Hericium erinaceus Extracts in Mouse Hippocampus after Pilocarpine-Induced Status Epilepticus

2019 ◽  
Vol 20 (4) ◽  
pp. 859 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Ji-Eun Kim ◽  
Kyoung Jeong ◽  
Sung Lim ◽  
Seong Kim ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Neuronal Death ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Brain Diseases ◽  
Cresyl Violet ◽  
Neuroprotective Effects ◽  
Hericium Erinaceus ◽  
Neuronal Nuclei ◽  
Underlying Mechanisms

Hericium erinaceus (HE), a culinary-medicinal mushroom, has shown therapeutic potential in many brain diseases. However, the role of HE in status epilepticus (SE)-mediated neuronal death and its underlying mechanisms remain unclear. We investigated the neuroprotective effects of HE using a pilocarpine-induced SE model. Male C57BL/6 mice received crude extracts of HE (60 mg/kg, 120 mg/kg, or 300 mg/kg, p.o.) for 21 d from 14 d before SE to 6 d after SE. At 7 d after SE, cresyl violet and immunohistochemistry of neuronal nuclei revealed improved hippocampal neuronal survival in animals treated with 60 mg/kg and 120 mg/kg of HE, whereas those treated with 300 mg/kg of HE showed similar neuronal death to that of vehicle-treated controls. While seizure-induced reactive gliosis, assessed by immunohistochemistry, was not altered by HE, the number of hippocampal cyclooxygenase 2 (COX2)-expressing cells was significantly reduced by 60 and 120 mg/kg of HE. Triple immunohistochemistry demonstrated no overlap of COX2 labeling with Ox42, in addition to a decrease in COX2/GFAP-co-immunoreactivity in the group treated with 60 mg/kg HE, suggesting that the reduction of COX2 by HE promotes neuroprotection after SE. Our findings highlight the potential application of HE for preventing neuronal death after seizures.

Neuroprotective effect of curcumin nanoparticles against rat model of status epilepticus induced by pilocarpine

2018 ◽  
Vol 15 (4) ◽  
Author(s):  
Yasser A. Khadrawy ◽  
Hussein G. Sawie ◽  
Eman N. Hosny
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Brain Regions ◽  
Necrosis Factor Alpha ◽  
Curcumin Nanoparticles ◽  
Tnf Α ◽  
Factor Alpha

Abstract Background The present study aims to investigate the neuroprotective effect of curcumin nanoparticles (Cur-NP) on the rat model of status epilepticus (SE) induced by pilocarpine. Methods In the present study, animals were divided into three groups: control animals, rat model of SE induced by a single dose of pilocarpine (380 mg/kg) injected intraperitoneally, and rat model of SE that received a daily intraperitoneal injection of Cur-NP (50 mg/kg) for four consecutive days prior to pilocarpine administration. Results The present results revealed a state of oxidative stress in the cortex and hippocampus of rat model of SE as compared to control. This was evident from the significant increase in lipid peroxidation and the significant decrease in reduced glutathione and nitric oxide. In addition, a significant increase in the levels of tumor necrosis factor-alpha (TNF-α) and caspase-3 was detected in the two studied brain regions of rat model of SE. The activities of acetylcholinesterase (AchE) and Na+/K+-ATPase decreased significantly in the cortex and hippocampus of rat model of SE. Protection with Cur-NP prevented oxidative stress and improved the elevated level of caspase-3 in the hippocampus and cortex and the hippocampal TNF-α to nonsignificant changes. Although Cur-NP prevented the decrease in AchE activity in the two studied brain regions, it failed to return Na+/K+-ATPase activity to its normal value. Conclusions It is clear from the present findings that Cur-NP could prevent the oxidative stress and neuroinflammation and cell death that were induced during SE. This in turn may help in ameliorating the subsequent cascades of events that follow SE and its development into epileptogenesis.

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