Neuroprotective role of glutathione peroxidase 4 in experimental subarachnoid hemorrhage models

Gao, Sheng-Qing; Liu, Jiaqiang; Han, Yanling; Deji, Qu-Zhen; Zhaba, Wang-Dui; Deng, Hong-Ji; Li, Xilin; Zhou, Meng-Liang

doi:10.1016/j.lfs.2020.118050

Cited by 28 publications

(26 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunofluorescence staining of brain sections was performed as described previously ( 15 ). Briefly, the brain sections were fixed in 4% paraformaldehyde.…”

Section: Methodsmentioning

confidence: 99%

“…The neurological scores were evaluated using the modified Garcia scoring system as previously described ( 15 ). Briefly, the evaluation scores ranged from 3–18 and were derived from six tests: spontaneous activity, symmetry in the movement of four limbs, forelimbs outstretching, climbing ability, body proprioception, and the response to vibrissae stimulation.…”

Section: Methodsmentioning

confidence: 99%

“…Western blotting was performed as described previously (15). B r i e fl y , e a c h b r a i n t i s s u e s a m p l e w a s l y s e d i n radioimmunoprecipitation assay buffer to blend 1% protease and phosphatase inhibitor cocktails.…”

Section: Western Blottingmentioning

confidence: 99%

See 2 more Smart Citations

A20 Establishes Negative Feedback With TRAF6/NF-κB and Attenuates Early Brain Injury After Experimental Subarachnoid Hemorrhage

et al. 2021

Self Cite

View full text Add to dashboard Cite

Nuclear factor (NF)-κB–ty -50mediated neuroinflammation plays a crucial role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). As an important negative feedback regulator of NF-κB, A20 is essential for inflammatory homeostasis. Herein, we tested the hypothesis that A20 attenuates EBI by establishing NF-κB–associated negative feedback after experimental SAH. In vivo and in vitro models of SAH were established. TPCA-1 and lentivirus were used for NF-κB inhibition and A20 silencing/overexpression, respectively. Cellular localization of A20 in the brain was determined via immunofluorescence. Western blotting and enzyme-linked immunosorbent assays were applied to observe the expression of members of the A20/tumor necrosis factor receptor-associated factor 6 (TRAF6)/NF-κB pathway and inflammatory cytokines (IL-6, IL-1β, TNF-α). Evans blue staining, TUNEL staining, Nissl staining, brain water content, and modified Garcia score were performed to evaluate the neuroprotective effect of A20. A20 expression by astrocytes, microglia, and neurons was increased at 24 h after SAH. A20 and inflammatory cytokine levels were decreased while TRAF6 expression was elevated after NF-κB inhibition. TRAF6, NF-κB, and inflammatory cytokine levels were increased after A20 silencing but suppressed with A20 overexpression. Also, Bcl-2, Bax, MMP-9, ZO-1 protein levels; Evans blue, TUNEL, and Nissl staining; brain water content; and modified Garcia score showed that A20 exerted a neuroprotective effect after SAH. A20 expression was regulated by NF-κB. In turn, increased A20 expression inhibited TRAF6 and NF-κB to reduce the subsequent inflammatory response. Our data also suggest that negative feedback regulation mechanism of the A20/TRAF6/NF-κB pathway and the neuroprotective role of A20 to attenuate EBI after SAH.

show abstract

“…Immunofluorescence staining of brain sections was performed as described previously ( 15 ). Briefly, the brain sections were fixed in 4% paraformaldehyde.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

A20 Establishes Negative Feedback With TRAF6/NF-κB and Attenuates Early Brain Injury After Experimental Subarachnoid Hemorrhage

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…Li et al ( Li Y. et al, 2021 ) found that inhibiting ferroptosis could ameliorate CD in the brain and neuronal death in the cell model by improving BBB permeability and cerebral edema, thus alleviating EBI after SAH. ACSL4 is able to induce ferroptosis, and increasing its expression would exacerbate inflammation, OS and cognitive deficits after SAH ( Qu et al, 2021 ); however, over-expression of GPX4, could reduce the brain water content and improve neurological behavior by suppressing ferroptosis ( Gao et al, 2020 ). Similarly, in in vivo experiments, Lip-1, a ferroptosis inhibitor, decreased neuronal death and neuro-inflammation in EBI by protecting mitochondrial functions and reducing lipid peroxidation, thereby ameliorating cerebral edema and neurological deficits after SAH ( Cao et al, 2021 ).…”

Section: Contribution Of Ferroptosis In Cardio-cerebrovascular Diseasementioning

confidence: 99%

Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases

Luo

Gong

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

The dynamic balance of cardiomyocytes and neurons is essential to maintain the normal physiological functions of heart and brain. If excessive cells die in tissues, serious Cardio-Cerebrovascular Diseases would occur, namely, hypertension, myocardial infarction, and ischemic stroke. The regulation of cell death plays a role in promoting or alleviating Cardio-Cerebrovascular Diseases. Ferroptosis is an iron-dependent new type of cell death that has been proved to occur in a variety of diseases. In our review, we focus on the critical role of ferroptosis and its regulatory mechanisms involved in Cardio-Cerebrovascular Diseases, and discuss the important function of ferroptosis-related inhibitors in order to propose potential implications for the prevention and treatment of Cardio-Cerebrovascular Diseases.

show abstract

“…In the subarachnoid hemorrhage (SAH) model, decreased GPX4 may play a major role in early brain injury after SAH. However, GPX4 overexpression significantly reduces lipid peroxidation and cell death and exerts a neuroprotective effect on SAH in vitro and in vivo (Gao et al, 2020). In the epileptic models, loss of hippocampal neurons may be due to reduced GPX4 expression, glutathione consumption, lipid peroxides, and iron accumulation (Qing et al, 2019).…”

Section: Zheng Et Al 2020mentioning

confidence: 99%

Iron Metabolism and Ferroptosis in Epilepsy

Chen

Zhang

et al. 2020

Front. Neurosci.

View full text Add to dashboard Cite

Epilepsy is a disease characterized by recurrent, episodic, and transient central nervous system (CNS) dysfunction resulting from an excessive synchronous discharge of brain neurons. It is characterized by diverse etiology, complex pathogenesis, and difficult treatment. In addition, most epileptic patients exhibit social cognitive impairment and psychological impairment. Iron is an essential trace element for human growth and development and is also involved in a variety of redox reactions in organisms. However, abnormal iron metabolism is associated with several neurological disorders, including hemorrhagic post-stroke epilepsy and post-traumatic epilepsy (PTE). Moreover, ferroptosis is also considered a new form of regulation of cell death, which is attributed to severe lipid peroxidation caused by the production of reactive oxygen species (ROS) and iron overload found in various neurological diseases, including epilepsy. Therefore, this review summarizes the study on iron metabolism and ferroptosis in epilepsy, in order to elucidate the correlation between iron and epilepsy. It also provides a novel method for the treatment, prevention, and research of epilepsy, to control epileptic seizures and reduce nerve injury after the epileptic seizure.

show abstract

Neuroprotective role of glutathione peroxidase 4 in experimental subarachnoid hemorrhage models

Cited by 28 publications

References 27 publications

A20 Establishes Negative Feedback With TRAF6/NF-κB and Attenuates Early Brain Injury After Experimental Subarachnoid Hemorrhage

A20 Establishes Negative Feedback With TRAF6/NF-κB and Attenuates Early Brain Injury After Experimental Subarachnoid Hemorrhage

Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases

Iron Metabolism and Ferroptosis in Epilepsy

Contact Info

Product

Resources

About