Microglial Activation and Oxidative Stress in PM2.5-Induced Neurodegenerative Disorders

Song, Jie; Han, Keyang; Wang, Ya; Qu, Rongrong; Liu, Yuan; Wang, Shaolan; Wang, Yinbiao; An, Zhen; Li, Juan; Wu, Hui; Wu, Weidong

doi:10.3390/antiox11081482

Cited by 17 publications

(14 citation statements)

References 115 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inflammation: PM 2.5 can activate the immune system, leading to the release of inflammatory cytokines and chemokines. Neurotoxicity: PM 2.5 exposure has been linked to neurotoxicity, including neuronal damage, neuroinflammation, and cognitive impairment [ 22 , 23 ]. In summary, PM 2.5 exposure can lead to various molecular and cellular mechanisms contributing to disease pathogenesis, including oxidative stress, inflammation, epigenetic modifications, mitochondrial dysfunction, autophagy impairment, and neurotoxicity.…”

Section: Neuroinflammation Toxicity and Neuroprotectionmentioning

confidence: 99%

“…Activation of AMPK by quercetin leads to the suppression of NF-kB and NLRP3 inflammasome activation, which in turn reduces inflammation in stroke. PM 2.5 -induced inflammation is associated with the activation of NF-kB and NLRP3 inflammasome, which produces pro-inflammatory cytokines and develops oxidative stress [ 22 , 84 , 85 , 86 ]. Quercetin has been shown to inhibit PM 2.5 -induced inflammation by inhibiting the activation of NF-kB and NLRP3 inflammasome through the AMPK signaling pathway [ 87 ].…”

Section: Quercetin Is An Anti-inflammatory Agent Via Ampk and Is Neur...mentioning

confidence: 99%

See 1 more Smart Citation

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

Chiang

Tsai

Wang

2023

IJMS

View full text Add to dashboard Cite

Neuroinflammation is a critical factor in developing and progressing numerous brain diseases, including neurodegenerative diseases. Chronic or excessive neuroinflammation can lead to neurotoxicity, causing brain damage and contributing to the onset and progression of various brain diseases. Therefore, understanding neuroinflammation mechanisms and developing strategies to control them is crucial for treating brain diseases. Studies have shown that neuroinflammation plays a vital role in the progression of neurodegenerative diseases, such as Alzheimer’s (AD) and Parkinson’s (PD), and stroke. Additionally, the effects of PM2.5 pollution on the brain, including neuroinflammation and neurotoxicity, are well-documented. Quercetin is a flavonoid, a plant pigment in many fruits, vegetables, and grains. Quercetin has been studied for its potential health benefits, including its anti-inflammatory, antioxidant, and anti-cancer properties. Quercetin may also have a positive impact on immune function and allergy symptoms. In addition, quercetin has been shown to have anti-inflammatory and neuroprotective properties and can activate AMP-activated protein kinase (AMPK), a cellular energy sensor that modulates inflammation and oxidative stress. By reducing inflammation and protecting against neuroinflammatory toxicity, quercetin holds promise as a safe and effective adjunctive therapy for treating neurodegenerative diseases and other brain disorders. Understanding and controlling the mechanisms of NF-κB and NLRP3 inflammasome pathways are crucial for preventing and treating conditions, and quercetin may be a promising tool in this effort. This review article aims to discuss the role of neuroinflammation in the development and progression of various brain disorders, including neurodegenerative diseases and stroke, and the impact of PM2.5 pollution on the brain. The paper also highlights quercetin’s potential health benefits and anti-inflammatory and neuroprotective properties.

show abstract

Section: Neuroinflammation Toxicity and Neuroprotectionmentioning

confidence: 99%

Section: Quercetin Is An Anti-inflammatory Agent Via Ampk and Is Neur...mentioning

confidence: 99%

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

Chiang

Tsai

Wang

2023

IJMS

View full text Add to dashboard Cite

show abstract

“…PM 2.5 can affect the central nervous system through multiple pathways and induce neuronal apoptosis to cause neurotoxicity (Song et al, 2022). In recent years, ferroptosis has been a new form of programmed death (Chen et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

PM_2.5 induces autophagy‐dependent ferroptosis by endoplasmic reticulum stress in SH‐SY5Y cells

Guo

Lyu

et al. 2023

J of Applied Toxicology

View full text Add to dashboard Cite

Fine particulate matter (PM2.5) has been a global environmental problem threatening public health in recent years. PM2.5 exposure was associated with an increased risk of neurodegenerative diseases related to neuronal apoptosis. Ferroptosis is a nonapoptotic form of programmed the cell death, characterized by excess iron‐dependent lipid peroxidation products. Whether PM2.5 could induce ferroptosis in cells and thus be involved in its neurotoxicity is unknown. In this study, we found that PM2.5 induced endoplasmic reticulum stress, apoptosis, autophagy, and ferroptosis in neuroblastoma human neuroblastoma cells (SH‐SY5Y). Interestingly, ferroptosis was the predominant form of mortality in the presence of high doses of PM2.5 exposure. In addition, the endoplasmic reticulum stress inhibitor 4‐phenylbutyric acid (4‐PBA) inhibited PM2.5‐induced cellular autophagy, apoptosis, and ferroptosis. Autophagy inhibitors chloroquine (CQ) alleviated PM2.5‐induced ferroptosis but did not reverse apoptosis. We also found that inhibition of both endoplasmic reticulum stress and autophagy reversed the PM2.5‐induced increase in the expression level of cytophagy nuclear receptor coactivator 4 (NCOA4). Our results suggested that PM2.5‐induced ferroptosis in SH‐SY5Y cells was autophagy‐dependent ferroptosis due to endoplasmic reticulum stress, which might be associated with the elevation of iron content caused by NCOA4‐mediated ferritin autophagy.

show abstract

“…In parallel with this, high expression levels of chemokines, interleukins, interferons, and tumor necrosis factor-α (TNF-α) have been discovered in the striatum and substantia nigra of PD post-mortem brain samples and CSF of AD patients (Hirsch and Hunot, 2009 ; Llano et al, 2012 ; Gelders et al, 2018 ). A neurotoxic microenvironment can be promoted by the continuous secretion of inflammatory mediators from microglia and astrocytes, thus facilitating neural degeneration, and glial cell death (Pardillo-Díaz et al, 2022 ; Song et al, 2022 ). In addition to apoptosis cell death, pyroptosis, a non-apoptotic programed cell death, can also occur in the CNS, which is mainly mediated by inflammatory processes.…”

Section: Neuroinflammation-induced Cell Death In Neurodegenerative Di...mentioning

confidence: 99%

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

Karvandi

Hesari

Aref

et al. 2023

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Neuronal loss is one of the striking causes of various central nervous system (CNS) disorders, including major neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and Amyotrophic lateral sclerosis (ALS). Although these diseases have different features and clinical manifestations, they share some common mechanisms of disease pathology. Progressive regional loss of neurons in patients is responsible for motor, memory, and cognitive dysfunctions, leading to disabilities and death. Neuronal cell death in neurodegenerative diseases is linked to various pathways and conditions. Protein misfolding and aggregation, mitochondrial dysfunction, generation of reactive oxygen species (ROS), and activation of the innate immune response are the most critical hallmarks of most common neurodegenerative diseases. Thus, endoplasmic reticulum (ER) stress, oxidative stress, and neuroinflammation are the major pathological factors of neuronal cell death. Even though the exact mechanisms are not fully discovered, the notable role of mentioned factors in neuronal loss is well known. On this basis, researchers have been prompted to investigate the neuroprotective effects of targeting underlying pathways to determine a promising therapeutic approach to disease treatment. This review provides an overview of the role of ER stress, oxidative stress, and neuroinflammation in neuronal cell death, mainly discussing the neuroprotective effects of targeting pathways or molecules involved in these pathological factors.

show abstract

Microglial Activation and Oxidative Stress in PM2.5-Induced Neurodegenerative Disorders

Cited by 17 publications

References 115 publications

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

PM_2.5 induces autophagy‐dependent ferroptosis by endoplasmic reticulum stress in SH‐SY5Y cells

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

Contact Info

Product

Resources

About

Microglial Activation and Oxidative Stress in PM2.5-Induced Neurodegenerative Disorders

Cited by 17 publications

References 115 publications

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

The Potential Benefits of Quercetin for Brain Health: A Review of Anti-Inflammatory and Neuroprotective Mechanisms

PM2.5 induces autophagy‐dependent ferroptosis by endoplasmic reticulum stress in SH‐SY5Y cells

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

Contact Info

Product

Resources

About

PM_2.5 induces autophagy‐dependent ferroptosis by endoplasmic reticulum stress in SH‐SY5Y cells