التفاصيل البيبلوغرافية
العنوان: |
Bilirubin Prevents the TH+ Dopaminergic Neuron Loss in a Parkinson’s Disease Model by Acting on TNF-α |
المؤلفون: |
Sri Jayanti, Rita Moretti, Claudio Tiribelli, Silvia Gazzin |
المصدر: |
International Journal of Molecular Sciences; Volume 23; Issue 22; Pages: 14276 |
بيانات النشر: |
Multidisciplinary Digital Publishing Institute |
سنة النشر: |
2022 |
المجموعة: |
MDPI Open Access Publishing |
مصطلحات موضوعية: |
tumor necrosis factor-alpha, neurodegenerative diseases, disease-modifying therapy, inflammation, redox, free bilirubin |
جغرافية الموضوع: |
agris |
الوصف: |
Parkinson’s disease (PD), the fastest-growing movement disorder, is still challenged by the unavailability of disease-modifying therapy. Mildly elevated levels of unconjugated bilirubin (UCB, PubChem CID 5280352) have been shown to be protective against several extra-CNS diseases, and the effect is attributed to its well-known anti-oxidant and anti-inflammatory capability. We explored the neuroprotective effect of low concentrations of UCB (from 0.5 to 4 µM) in our PD model based on organotypic brain cultures of substantia nigra (OBCs-SN) challenged with a low dose of rotenone (Rot). UCB at 0.5 and 1 µM fully protects against the loss of TH+ (dopaminergic) neurons (DOPAn). The alteration in oxidative stress is involved in TH+ positive neuron demise induced by Rot, but is not the key player in UCB-conferred protection. On the contrary, inflammation, specifically tumor necrosis factor alpha (TNF-α), was found to be the key to UCB protection against DOPAn sufferance. Further work will be needed to introduce the use of UCB into clinical settings, but determining that TNF-α plays a key role in PD may be crucial in designing therapeutic options. |
نوع الوثيقة: |
text |
وصف الملف: |
application/pdf |
اللغة: |
English |
Relation: |
Biochemistry; https://dx.doi.org/10.3390/ijms232214276 |
DOI: |
10.3390/ijms232214276 |
الاتاحة: |
https://doi.org/10.3390/ijms232214276 |
Rights: |
https://creativecommons.org/licenses/by/4.0/ |
رقم الانضمام: |
edsbas.8C695085 |
قاعدة البيانات: |
BASE |