Overexpression of the Aryl Hydrocarbon Receptor (Ahr) Mediates an Oxidative Stress Response following Injection of Fine Particulate Matter in the Temporal Cortex
| Autor: | So Min Lee, Sohyeon Park, Moo Kyun Park, Kyung Woon Kim, Da hye Lee, So Young Kim, Bu Soon Son |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Aging medicine.medical_specialty Article Subject CYP1B1 medicine.disease_cause Biochemistry RAGE (receptor) Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Internal medicine Cytochrome P-450 CYP1A1 medicine Animals Receptor Brevican Temporal cortex QH573-671 biology Chemistry Cell Biology General Medicine Aryl hydrocarbon receptor Temporal Lobe Rats Nitric oxide synthase Oxidative Stress 030104 developmental biology Endocrinology Gene Expression Regulation Receptors Aryl Hydrocarbon Cytochrome P-450 CYP1B1 biology.protein Female Particulate Matter Cytology 030217 neurology & neurosurgery Oxidative stress Research Article |
| Zdroj: | Oxidative Medicine and Cellular Longevity Oxidative Medicine and Cellular Longevity, Vol 2020 (2020) |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | Studies have shown that particulate matter (PM) induces the expression of the aryl hydrocarbon receptor (Ahr) leading to the activation of the oxidative stress response. This study is aimed at characterizing the specific impact of fine PM on the expression profile of the Ahr and oxidative stress response in the primary auditory cortex. PM2.5 ( n = 14 per group), respectively. One week after intracranial injection, the temporal cortex was harvested. Transmission electron microscopy was performed to evaluate the distribution of PM2.5 within the temporal cortex. Additionally, the mRNA and protein expression levels of cytochrome P450 1A1 (CYP1A1), CYP1B1, inducible nitric oxide synthase (iNOS), Ahr, and brevican mRNA and protein were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) or western blotting, respectively. Finally, the protein expression levels of the receptor for advanced glycation end products (RAGE) were estimated using enzyme-linked immunosorbent assay (ELISA). PM2.5 was observed in intracellular vesicles within the temporal cortex following intracranial injection. Levels of oxidative stress molecules (i.e., CYP1A1, CYP1B1, and iNOS), Ahr, Brevican, and RAGE were higher in the PM2.5 group compared with the control group. Intracranial administration of PM2.5 led to increased levels of Ahr and markers of an oxidative stress response in the temporal cortex. The oxidative stress response-mediated increases in the levels of brevican and RAGE. |
| Databáze: | OpenAIRE |
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