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SCIENTIFIC LITERATURE · MED

⁇ i>Nigella sativa ⁇ /i> Yağ LPS-İndüklenmiş Mikroglial Enflamasyonu Azaltır: ⁇ i>M ⁇ /i> ⁇ sub>1 ⁇ /sub>/ ⁇ i> ⁇ sub> Denge Üzerine Bir Değerlendirme.

<i>Nigella sativa</i> Oil Reduces LPS-Induced Microglial Inflammation: An Evaluation on <i>M</i> <sub>1</sub>/<i>M</i> <sub>2</sub> Balance.

Makine çevirisi · Editoryal inceleme bekliyor

Evid Based Complement Alternat Med · 2022-06-14

DOI: 10.1155/2022/5639226PMID: 35747373

Open accessresearch-article; Journal ArticleKaynağa git ↗

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ObjectivesThe immune system plays a critical defence role against infections, injuries, and carcinogenic stimuli. As the macrophages of the brain resides in the innate immune system, microglia and their polarisation (M 1/M 2) play regulatory roles in inflammation in CNS, such as Parkinson's, Alzheimer's, dementia complex, and multiple sclerosis. Nigella sativa belongs to the Ranunculaceae family and has different anti-inflammatory and antioxidant effects. We conducted this study to evaluate the anti-inflammatory and protective properties of N. sativa oil (NSO) on the microglial cells and their polarisation (M 1/M 2) in the presence of LPS as a model of neuroinflammation.MethodsThe protective effects of NSO (10-40 µg/ml) were studied on the LPS-induced microglial cells, and the levels of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, prostaglandin E2 (PGE2), and IL-10 were evaluated using both ELISA and gene expression methods. The levels of cyclooxygenase-2 (COX-2), inducible NOS (iNOS), and arginase-1 (Arg1) were also evaluated using the real-time PCR method. In addition, nitrite oxide (NO) and urea were measured using biochemical methods.ResultsNSO decreased LPS-induced toxicity at all doses (P μg/ml) also significantly reduced the levels of TNF-α, PGE2, IL-1β, and IL-6 in the presence of LPS (P P P P ConclusionNSO attenuated LPS-induced inflammation and increased microglia's anti-inflammatory status. These results may prove that NSO is potentially an immunomodulator for various neurodegenerative diseases by M1 phenotype dominancy, such as Alzheimer's and Parkinson's diseases.

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