| Autor: |
Song, Jie, Han, Keyang, Wang, Ya, Qu, Rongrong, Liu, Yuan, Wang, Shaolan, Wang, Yinbiao, An, Zhen, Li, Juan, Wu, Hui, Wu, Weidong |
| Předmět: |
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| Zdroj: |
Antioxidants; Aug2022, Vol. 11 Issue 8, pN.PAG-N.PAG, 23p |
| Abstrakt: |
The four critical issues are of significant relevance and need to be addressed: (1) The routes through which PM SB 2.5 sb access CNS; (2) the receptors microglia use to relay PM SB 2.5 sb neurotoxic signals; (3) PM SB 2.5 sb -induced microglial oxidative stress; and (4) the interactions between microglia and neurons. In addition, a study revealed that microglia cultures derived from mice missing functional NADPH oxidase, the enzyme responsible for microglial extracellular superoxide production, were insensitive to DEP-induced neurotoxicity, indicating that microglia-derived ROS are key for DEP-induced DA neurotoxicity [[100]]. Keywords: PM2.5; microglia; oxidative stress; neuroinflammation; neurodegeneration EN PM2.5 microglia oxidative stress neuroinflammation neurodegeneration N.PAG N.PAG 23 08/29/22 20220801 NES 220801 1. Pre-treatment with fractalkine (50 pg/mL), a chemokine from neurons as a soluble anti-inflammatory signal for microglia [[102]], ameliorated DEP (50 g/mL)-induced H SB 2 sb O SB 2 sb production from microglia and protected against DEP-induced DA neurotoxicity in midbrain neuron-glia cultures [[84]]. In the presence of primary cortical microglia neuronal cell death increased by 2-3 fold after co-treatment with DEP, suggesting that microglia are important contributors to DEP-induced CGN neurotoxicity, possibly due to soluble intermediates since microglia-conditioned medium by DEP treatment was also toxic to CGNs [[101]]. [Extracted from the article] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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