Ferulic acid attenuates oxidative DNA damage and inflammatory responses in microglia induced by benzo(a)pyrene

Bao, Yongping; Chen, Qingjie; Xie, Yushuang; Tao, Zhe; Jin, Ketao; Chen, Shuli; Bai, Y.; Yang, Jun; Song, Shuai

doi:10.1016/j.intimp.2019.105980

Cited by 47 publications

(14 citation statements)

References 61 publications

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“…44 Overactivation of microglia disturbs the spinal microenvironment and triggers inappropriate inflammatory responses, which aggravate in neural dysfunction after SCI. Some studies have indicated that FA inhibits the microglia-mediated proinflammatory response and thus may exert neuroprotective effects, 45 which is consistent with our results showing that FOs downregulate the expression of TNF-α, IL-1α, and IL-6 and decrease the number of microglial cells in spinal cord lesions after contusion injury. In addition, IL-1α and TNF-α secreted by microglia play an important role in activating A1 astrocytes, which do not promote neuronal survival, synaptogenesis, or phagocytosis but induce neuronal death and demyelination.…”

Section: ■ Discussionsupporting

confidence: 93%

Feruloylated Oligosaccharides Alleviate Central Nervous Inflammation in Mice Following Spinal Cord Contusion

Huang

et al. 2020

J. Agric. Food Chem.

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As one of the empirical models of the chronic central inflammatory response, a spinal cord injury (SCI) deteriorates the neuronal survival and results in irreversible motor and sensory dysfunction below the injury area. Our previous studies have reported that maize bran feruloylated oligosaccharides (FOs) exert significant anti-inflammatory activities both in diabetes and colitis. However, no direct evidence of FOs alleviating central nervous inflammation was stated. This study aimed to investigate the therapeutic effect of FOs on SCI and its potential mechanism. Our results indicated that 4 weeks of FO administration effectively mitigated the inflammatory response via decreasing the number of microglia (labelled with Iba1), result in the expression of IL-1α, IL-2, IL-6, IL-18 and TNF-α downregulating, but the level of IL-10 and BDNF increases in the injured spinal cord. Moreover, FOs enhanced neuronal survival, ameliorated the scar cavities, and improved behaviors, including Basso mouse scale (BMS) scores and the gait of mice after SCI. Together, these results demonstrated that administration of FOs showed superior functional recovery effects in a SCI model. Also, FOs may modulate inflammatory activities by regulating the expression of proinflammatory factors, decreasing the production of inflammatory cells, and promoting functional recovery through the MAPK pathway following SCI.

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Section: ■ Discussionsupporting

confidence: 93%

Feruloylated Oligosaccharides Alleviate Central Nervous Inflammation in Mice Following Spinal Cord Contusion

Huang

et al. 2020

J. Agric. Food Chem.

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“…The cytotoxicity of BaP is related to its proin ammatory effect.Present studies suggest that BaP increases ROS production,and the NOD-like receptor(NLR) family pyrin domain-containing 3(NLRP3) signaling pathway is involved in the toxic effect of BaP (Bao 2019). NLRP3 in ammasome also plays an important role in BaP induced lung tumorigenesis,and NLRP3 deletion signi cantly inhibits this process(Li 2021), .Coincidently,we conducted high-throughput sequencing on the MI injury area and then found that the NOD-like receptor signaling pathway appeared in both top 20 of KEGG enrichment and top 20 of GO enrichment,suggesting that NLRP3 in ammasome cannot be ignored in the mechanism of BaP aggravating MI injury.Pyroptosis is a form of lytic programmed cell death initiated by NLRP3 in ammasome (Kovacs 2017).…”

Section: Discussionmentioning

confidence: 99%

3,4-benzo[a]pyrene aggravates myocardial infarction injury by activating NLRP3-related pyroptosis through PINK1/Parkin-mitophagy-mPTP opening axis

Xiang

et al. 2022

Preprint

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Acute myocardial infarction(AMI) accounts for more than one third of ischemic heart disease deaths. Air pollution exposure,even for a short-term exposure,is conspicuously relevant to increased risk of MI mortality and clinical evidence has showed that air pollution particulate matter(PM) induces the aggravation of AMI.3,4-benzo[a]pyrene(BaP),a polycyclic aromatic hydrocarbon(PAH) with toxicity,is a typical air pollutant present in PM and is often measured as the representative of PAHs.The purpose of this study was to investigate whether BaP can aggravate myocardial infarction(MI) injury and,on this basis,to investigate the relevant mechanisms.The MI mouse model and the oxygen and glucose deprivation(OGD) H9C2 cell model were used to investigate the effect of BaP in MI injury.The involvement of mitophagy and NLRP3-related pyroptosis in regulating deterioration of cardiac function and aggravation of MI injury induced by BaP was comprehensively evaluated.Our study showed that BaP can aggravate MI injury in vivo and in vitro,and this result was based on NLRP3-related pyroptosis induced by BaP.In addition,BaP can inhibit PINK1/Parkin dependent mitophagy through the aryl hydrocarbon receptor(AhR),thus inducing mitochondrial permeability transition pore(mPTP) opening.Our results suggested a role for the BaP from air pollution in the aggravation of MI injury and revealed that BaP aggravates MI injury by activating NLRP3-related pyroptosis through PINK1/Parkin-mitophagy-mPTP opening axis.

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“…Subchronic oral administration of BaP (2 mg/kg/day for 28 days) causes astroglial reaction and motor/cognitive impairments in rats [54]. A previous study has shown that treatment of BV2 (mouse microglial cell line) with BaP (10 μM) triggered inflammatory responses, such as upregulation of iNOS and cyclooxygenase-2 (COX-2) as well as production of multiple pro-inflammatory factors including nitric oxide (NO), reactive oxygen species (ROS), IL-1β, and IL-6 [55]. Benzo[a]pyrene diol epoxide, the major metabolite of BaP, has been shown to upregulate COX-2 expression in rat astroglia [56].…”

Section: Discussionmentioning

confidence: 99%

Benzo(a)pyrene exposure induced neuronal loss, plaque deposition, and cognitive decline in APP/PS1 mice

Liú¹,

Zhao²,

Qi³

et al. 2020

J Neuroinflammation

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Background: Exposure to benzo(a)pyrene (BaP) was associated with cognitive impairments and some Alzheimer's disease (AD)-like pathological changes. However, it is largely unknown whether BaP exposure participates in the disease progression of AD. Objectives: To investigate the effect of BaP exposure on AD progression and its underlying mechanisms. Methods: BaP or vehicle was administered to 4-month-old APPswe/PS1dE9 transgenic (APP/PS1) mice and wildtype (WT) mice for 2 months. Learning and memory ability and exploratory behaviors were evaluated 1 month after the initiation/termination of BaP exposure. AD-like pathological and biochemical alterations were examined 1 month after 2-month BaP exposure. Levels of soluble beta-amyloid (Aβ) oligomers and the number of Aβ plaques in the cortex and the hippocampus were quantified. Gene expression profiling was used to evaluate alternation of genes/pathways associated with AD onset and progression. Immunohistochemistry and Western blot were used to demonstrate neuronal loss and neuroinflammation in the cortex and the hippocampus. Treatment of primary neuron-glia cultures with aged Aβ (a mixture of monomers, oligomers, and fibrils) and/or BaP was used to investigate mechanisms by which BaP enhanced Aβ-induced neurodegeneration. Results: BaP exposure induced progressive decline in spatial learning/memory and exploratory behaviors in APP/PS1 mice and WT mice, and APP/PS1 mice showed severer behavioral deficits than WT mice. Moreover, BaP exposure promoted neuronal loss, Aβ burden and Aβ plaque formation in APP/PS1 mice, but not in WT mice. Gene expression profiling showed most robust alteration in genes and pathways related to inflammation and immunoregulatory process, Aβ secretion and degradation, and synaptic formation in WT and APP/PS1 mice after BaP exposure. Consistently, the cortex and the hippocampus of WT and APP/PS1 mice displayed activation of microglia and astroglia and upregulation of inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP), and NADPH oxidase (three widely used neuroinflammatory markers) after BaP exposure. Furthermore, BaP exposure aggravated neurodegeneration induced by aged Aβ peptide in primary neuron-glia cultures through enhancing NADPH oxidase-derived oxidative stress.

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Ferulic acid attenuates oxidative DNA damage and inflammatory responses in microglia induced by benzo(a)pyrene

Cited by 47 publications

References 61 publications

Feruloylated Oligosaccharides Alleviate Central Nervous Inflammation in Mice Following Spinal Cord Contusion

Feruloylated Oligosaccharides Alleviate Central Nervous Inflammation in Mice Following Spinal Cord Contusion

3,4-benzo[a]pyrene aggravates myocardial infarction injury by activating NLRP3-related pyroptosis through PINK1/Parkin-mitophagy-mPTP opening axis

Benzo(a)pyrene exposure induced neuronal loss, plaque deposition, and cognitive decline in APP/PS1 mice

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