Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway
Yue song Zhao, Jun yan Li, Zhao cong Li, Lei lei Wang, Cui liu Gan, Jing Chen, Si yang Jiang, Michael Aschner, Shi yan Ou, Yue ming Jiang
Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1β levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.
Neurochemical Research
BDNF
PAS-Na
SIRT1/HMGB1/NF-κB pathway
Dive into the research topics of 'Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway'. Together they form a unique fingerprint.
Aminosalicylic Acid Medicine & Life Sciences 100%
Brain-Derived Neurotrophic Factor Medicine & Life Sciences 64%
Cerebral Cortex Medicine & Life Sciences 56%
Anti-Inflammatory Agents Medicine & Life Sciences 45%
Antiinflammatory Chemical Compounds 39%
Interleukin-1beta Medicine & Life Sciences 38%
Zhao, Y. S., Li, J. Y., Li, Z. C., Wang, L. L., Gan, C. L., Chen, J., Jiang, S. Y., Aschner, M., Ou, S. Y., & Jiang, Y. M. (2023). Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway. Neurochemical Research, 48(1), 238-249. https://doi.org/10.1007/s11064-022-03739-1
Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway. / Zhao, Yue song; Li, Jun yan; Li, Zhao cong et al.
In: Neurochemical Research, Vol. 48, No. 1, 01.2023, p. 238-249.
Zhao, YS, Li, JY, Li, ZC, Wang, LL, Gan, CL, Chen, J, Jiang, SY, Aschner, M, Ou, SY & Jiang, YM 2023, 'Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway', Neurochemical Research, vol. 48, no. 1, pp. 238-249. https://doi.org/10.1007/s11064-022-03739-1
Zhao YS, Li JY, Li ZC, Wang LL, Gan CL, Chen J et al. Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway. Neurochemical Research. 2023 Jan;48(1):238-249. doi: 10.1007/s11064-022-03739-1
Zhao, Yue song ; Li, Jun yan ; Li, Zhao cong et al. / Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway. In: Neurochemical Research. 2023 ; Vol. 48, No. 1. pp. 238-249.
@article{bd2167823a344a9496385226b02c0384,
title = "Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway",
abstract = "Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1β levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.",
keywords = "BDNF, Lead, Neuroinflammation, PAS-Na, SIRT1/HMGB1/NF-κB pathway",
author = "Zhao, {Yue song} and Li, {Jun yan} and Li, {Zhao cong} and Wang, {Lei lei} and Gan, {Cui liu} and Jing Chen and Jiang, {Si yang} and Michael Aschner and Ou, {Shi yan} and Jiang, {Yue ming}",
note = "Funding Information: Funding support was provided by grants from the National Natural Science Foundation of China (Grant No. NSFC 81773476). Funding Information: The authors thank Dr. Yan Li from Guangxi Zhuang Autonomous Region Institute for the Prevention and Treatment of Occupational Disease for her help in the detection of cerebral cortex Pb levels. Publisher Copyright: {\textcopyright} 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.",
journal = "Neurochemical Research",
T1 - Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway
AU - Zhao, Yue song
AU - Li, Jun yan
AU - Li, Zhao cong
AU - Wang, Lei lei
AU - Gan, Cui liu
AU - Chen, Jing
AU - Jiang, Si yang
AU - Aschner, Michael
AU - Ou, Shi yan
AU - Jiang, Yue ming
N1 - Funding Information: Funding support was provided by grants from the National Natural Science Foundation of China (Grant No. NSFC 81773476). Funding Information: The authors thank Dr. Yan Li from Guangxi Zhuang Autonomous Region Institute for the Prevention and Treatment of Occupational Disease for her help in the detection of cerebral cortex Pb levels. Publisher Copyright: © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
N2 - Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1β levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.
AB - Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1β levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.
KW - BDNF
KW - Lead
KW - Neuroinflammation
KW - PAS-Na
KW - SIRT1/HMGB1/NF-κB pathway
JO - Neurochemical Research
JF - Neurochemical Research