Arc regulates brain damage and neuroinflammation via Sirt1 signaling following subarachnoid hemorrhage

Chen, Tao; Xu, Ye-Ping; Chen, Yang; Sun, Shu; Yan, Zhi-Zhong; Wang, Yu-Hai

doi:10.1016/j.brainresbull.2023.110780

Cited by 6 publications

(3 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both ARC and EGR2 have also been associated with Nrf2 (Nuclear factor erythroid-2 related factor 2), a transcription factor involved in the regulation of antioxidant and inflammatory responses. Specifically, knockdown of ARC has been demonstrated to inhibit Nrf2 expression [45]. And is increased in parallel to Nrf2 in transgenic animals less prone to oxidative stress [46], whereas parallel increases in EGR2 and Nrf2 are associated with improved retention memory [47].…”

Section: Discussionmentioning

confidence: 99%

Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes

Kulbe,

Nguyen,

et al. 2023

Brain Sciences

View full text Add to dashboard Cite

E-cigarette use has been marketed as a safer alternative to traditional cigarettes, as a means of smoking cessation, and are used at a higher rate than the general population in people with HIV (PWH). Early growth receptor 2 (EGR2) and Activity-Regulated Cytoskeleton-Associated Protein (ARC) have a role in addiction, synaptic plasticity, inflammation, and neurodegeneration. This study showed that 10 days of exposure to e-cigarette vapor altered gene expression in the brains of 6-month-old, male, Sprague Dawley rats. Specifically, the e-cigarette solvent vapor propylene glycol (PG) downregulated EGR2 and ARC mRNA expression in frontal cortex, an effect which was reversed by nicotine (NIC) and THC, suggesting that PG could have a protective role against NIC and cannabis dependence. However, in vitro, PG upregulated EGR2 and ARC mRNA expression at 18 h in cultured C6 rat astrocytes suggesting that PG may have neuroinflammatory effects. PG-induced upregulation of EGR2 and ARC mRNA was reversed by NIC but not THC. The HIV antiretroviral DTG reversed the effect NIC had on decreasing PG-induced upregulation of EGR2, which is concerning because EGR2 has been implicated in HIV latency reversal, T-cell apoptosis, and neuroinflammation, a process that underlies the development of HIV-associated neurocognitive disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes

Kulbe,

Nguyen,

et al. 2023

Brain Sciences

View full text Add to dashboard Cite

show abstract

“…Additionally, it has been demonstrated that two SIRT1 agonists, astaxanthin and berberine, promote cognitive and memory recovery in mice through the SIRT1/p38 MAPK pathway [70,75]. Furthermore, the SIRT1/Nrf2 pathway mitigates ferroptosis after brain injury by activating GPX4, a key factor in ferroptosis [76,77]. Upregulation of SIRT1 can reverse the decrease in GPX4 content in the hippocampus after ischemic hypoxic injury, which is an important treatment target for HIBI [76].…”

Section: The Link Between Neuroinflammation and Ferroptosismentioning

confidence: 99%

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Xu,

Jia,

et al. 2024

Antioxidants

View full text Add to dashboard Cite

Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers’ findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders.

show abstract

“…[8][9][10] Previous studies have shown that SIRT1 can not only be expressed in microglia, but also participate in neuroprotective effects by regulating microglia function in SAH. Chen et al 11 used 2,3,5,6-tetramethylpyrazine to activate SIRT1 in BV2 cell, which alleviated neuroinflammation after SAH by inhibiting M1 microglial polarization; Arc could regulate brain injury and neuroinflammation after SAH through SIRT1 in a SAH mouse; 12 in addition, SIRT1 could promote M2 microglia polarization by reducing ROS-mediated NLRP3 inflammasome signaling and alleviate neuroinflammatory damage after SAH. 13 What's more, SIRT1 can also play a role in the central nervous system by participating in regulating mitophagy.…”

Section: Introductionmentioning

confidence: 99%

NAD-Dependent Protein Deacetylase Sirtuin-1 Mediated Mitophagy Regulates Early Brain Injury After Subarachnoid Hemorrhage

Wang,

Lin

2024

JIR

View full text Add to dashboard Cite

Background This study focuses on the role of SIRT1 in neuroinflammation caused by early brain injury (EBI) after subarachnoid hemorrhage (SAH), and explores its mechanism in mitophagy after SAH. Methods C57BL/6J mice and primary microglia SAH in vivo and in vitro models were constructed to explore the expression level of SIRT1 in neuroinflammation after SAH. Subsequently, the brain edema content, blood–brain barrier (BBB) damage and neurological function scores of the mice were observed after using the SIRT1 inhibitor EX-527. q-PCR and Western blot were used to detect relevant genes and proteins, and enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of IL-6, IL-1β, and TNF-α inflammatory factors. Immunofluorescence staining was used to observe the positive level of SIRT1 and the degree of mitochondria-lysosome fusion, and transmission electron microscopy was used to observe mitochondrial damage and autophagosome levels. Results In in vivo and in vitro experiments, we found that SIRT1 expression increased after SAH, and neurological deficits, brain edema, and blood–brain barrier damage after SAH were aggravated. Inhibiting SIRT1 further aggravates the aforementioned damage. In addition, EX-527 can also inhibit the level of mitophagy and aggravate neuroinflammation after SAH. Conclusion Our results indicated that SIRT1 promotes mitophagy and alleviates neuroinflammation after SAH.

show abstract

Arc regulates brain damage and neuroinflammation via Sirt1 signaling following subarachnoid hemorrhage

Cited by 6 publications

References 40 publications

Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes

Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

NAD-Dependent Protein Deacetylase Sirtuin-1 Mediated Mitophagy Regulates Early Brain Injury After Subarachnoid Hemorrhage

Contact Info

Product

Resources

About