Melatonin Attenuates Ropivacaine-Induced Apoptosis by Inhibiting Excessive Mitophagy Through the Parkin/PINK1 Pathway in PC12 and HT22 Cells

Inflammation ◽  
2022 ◽  
Author(s):  
Lian Zeng ◽  
Jiafeng He ◽  
Chenguang Liu ◽  
Fuyu Zhang ◽  
Zhen Zhang ◽  
...  
Keyword(s):  
Ht22 Cells ◽  
Induced Apoptosis

scholarly journals Ephrin-B2 inhibits Aβ25-35-induced apoptosis by alleviating endoplasmic reticulum stress and promoting autophagy in HT22 cells

2019 ◽  
Vol 704 ◽  
pp. 50-56
Author(s):  
Shuzhi Zhong ◽  
Dong Pei ◽  
Lei Shi ◽  
Yong Cui ◽  
Zongyuan Hong
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Ht22 Cells ◽  
Induced Apoptosis

scholarly journals Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Mei-Hua Jin ◽  
Jia-Bin Yu ◽  
Hu-Nan Sun ◽  
Ying-Hua Jin ◽  
Gui-Nan Shen ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ht22 Cells ◽  
Apoptotic Protein ◽  
Intracellular Ros ◽  
Induced Apoptosis ◽  
The Brain

Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present study, we observed significant increasing of intracellular ROS accumulations in Peroxiredoxin II (Prx II) knockdown HT22 cells, which were induced by alcohol treatments. We also found that the level of ROS in mitochondrial was also increased, resulting in a decrease in the mitochondrial membrane potential. The phosphorylation of GSK3β (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3β in Prx II knockdown HT22 cells. Moreover, NAC treatment also dramatically restored the mitochondrial membrane potential and the cellular apoptosis in Prx II knockdown HT22 cells. Our findings suggest that Prx II plays a crucial role in alcohol-induced neuronal cell apoptosis by regulating the cellular ROS levels, especially through regulating the ROS-dependent mitochondrial membrane potential. Consequently, Prx II may be a therapeutic target molecule for alcohol-induced neuronal cell death, which is closely related to ROS-dependent mitochondria dysfunction.

Blockade of SOCE protects HT22 cells from hydrogen peroxide-induced apoptosis

2013 ◽  
Vol 441 (2) ◽  
pp. 351-356 ◽  
Author(s):  
Wei Rao ◽  
Lei Zhang ◽  
Ning Su ◽  
Kai Wang ◽  
Hao Hui ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Ht22 Cells ◽  
Induced Apoptosis

scholarly journals Curcumin abates hypoxia-induced oxidative stress based-ER stress-mediated cell death in mouse hippocampal cells (HT22) by controlling Prdx6 and NF-κB regulation

2013 ◽  
Vol 304 (7) ◽  
pp. C636-C655 ◽  
Author(s):  
Bhavana Chhunchha ◽  
Nigar Fatma ◽  
Eri Kubo ◽  
Prerana Rai ◽  
Sanjay P. Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Er Stress ◽  
Molecular Mechanisms ◽  
Stress Proteins ◽  
Ht22 Cells ◽  
Peroxiredoxin 6 ◽  
Homologous Protein ◽  
Survival Signaling ◽  
Induced Apoptosis

Oxidative stress and endoplasmic reticulum (ER) stress are emerging as crucial events in the etiopathology of many neurodegenerative diseases. While the neuroprotective contributions of the dietary compound curcumin has been recognized, the molecular mechanisms underlying curcumin's neuroprotection under oxidative and ER stresses remains elusive. Herein, we show that curcumin protects HT22 from oxidative and ER stresses evoked by the hypoxia (1% O2 or CoCl2 treatment) by enhancing peroxiredoxin 6 (Prdx6) expression. Cells exposed to CoCl2 displayed reduced expression of Prdx6 with higher reactive oxygen species (ROS) expression and activation of NF-κB with IκB phosphorylation. When NF-κB activity was blocked by using SN50, an inhibitor of NF-κB, or cells treated with curcumin, the repression of Prdx6 expression was restored, suggesting the involvement of NF-κB in modulating Prdx6 expression. These cells were enriched with an accumulation of ER stress proteins, C/EBP homologous protein (CHOP), GRP/78, and calreticulin, and had activated states of caspases 12, 9, and 3. Reinforced expression of Prdx6 in HT22 cells by curcumin reestablished survival signaling by reducing propagation of ROS and blunting ER stress signaling. Intriguingly, knockdown of Prdx6 by antisense revealed that loss of Prdx6 contributed to cell death by sustaining enhanced levels of ER stress-responsive proapoptotic proteins, which was due to elevated ROS production, suggesting that Prdx6 deficiency is a cause of initiation of ROS-mediated ER stress-induced apoptosis. We propose that using curcumin to reinforce the naturally occurring Prdx6 expression and attenuate ROS-based ER stress and NF-κB-mediated aberrant signaling improves cell survival and may provide an avenue to treat and/or postpone diseases associated with ROS or ER stress.

scholarly journals Ishige okamurae Suppresses Trimethyltin-Induced Neurodegeneration and Glutamate-Mediated Excitotoxicity by Regulating MAPKs/Nrf2/HO-1 Antioxidant Pathways

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 440
Author(s):  
Oh Yun Kwon ◽  
Seung Ho Lee
Keyword(s):  
Molecular Mechanisms ◽  
Long Term Memory ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ht22 Cells ◽  
Ishige Okamurae ◽  
Mapk Inhibitors ◽  
Induced Apoptosis

Many neurodegenerative diseases have several similar cellular dysregulations. We investigated the inhibitory role of Ishige okamurae, an edible brown alga, on neurodegenerative processes by estimating the effects of Ishige okamurae on excitotoxicity induced by glutamate in vitro and neurodegeneration induced by trimethyltin (TMT) in vivo. This study aimed to describe the molecular mechanisms responsible for the mediating anti-neurodegenerative effects of Ishige okamurae extract (IOE). The oral administration of IOE to TMT-injected mice impeded the TMT-mediated short- and long-term memory impairments investigated by the Morris water maze and Y-maze test. IOE attenuated TMT-mediated cellular apoptosis and the expression of brain-derived neurotrophic factor, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) in mice brains. Glutamate-induced apoptosis and the expression of reactive oxygen species, Nrf2, and HO-1 in HT22 cells were also attenuated by IOE. In addition, TMT- and glutamate-induced phosphorylation of mitogen-activated protein kinases (MAPKs) in mouse brain tissues and HT22 cells were attenuated by the treatment of IOE. In HT22 cells, administration of MAPK inhibitors recovered the glutamate induced by the expression of Nrf2, HO-1, and cellular dysregulation to the equal extent to IOE administration. Taken together, these results suggest that IOE could attenuate neurodegenerative processes, such as TMT- and glutamate-mediated neuronal dysregulation, by regulating MAPKs/Nrf-2/HO-1 antioxidant pathways.

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