INSL3 suppresses LPS-induced inflammation in N9 microglia cells

Dilek Şaker; Gülfidan Coşkun; Sait Polat

Makale detayları

INSL3 suppresses LPS-induced inflammation in N9 microglia cells

Yazarlar:

Dilek Şaker | Gülfidan Coşkun | Sait Polat

Yayıncı:

Cukurova University

Ana Başlıklar:

Hücresel İmmünoloji | İmmünoloji (Diğer)

Dergi:

Cukurova Medical Journal Vol.49 Issue 2, pp.489-496

Belge Tipi:

Makale

Yayın Tarihi:

6/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001320801

pISSN:

2602-3032

Anahtar kelimeler:

Özet:

 Purpose: The G-protein coated receptor GPCR family, including the Insulin-Like Peptide 3 INSL3 receptor, is involved in the Nuclear Factor kappa B NF-κB-mediated pathway in inflammation. In this regard, it can be thought that INSL3 plays a role in inflammation via the NF-κB pathway. In this study, we investigated the effect of INSL3 on inflammation and cell viability in the lipopolysaccharide LPS-induced N9 microglia cell line. Materials and Methods: N9 microglial cells were pretreated with INSL3 for 2 hours, and then treated with LPS for 6 hours. Cell viability was identified by WST-8 assay. Immunostaining was performed to evaluate the levels of Interleukin-1β IL-1β, Tumor necrosis factor TNF-α, and NF-κB. Results: The cells in the LPS group showed degenerative changes in morphology and decreased cell viability. In the INSL3LPS group 1.210.06, the general appearance and viability of the cells were more similar to the control group 1.920.04 compared to the LPS group 0.610.05. It was determined that INSL3 prevented the LPS-induced increase in IL-1β, TNF-α, and NF-κB levels and decreased cell death. Conclusion: INSL3 suppresses inflammation and thus promotes cellular healing and can be considered a therapeutic agent that reduces inflammation.

 Purpose: The G-protein coated receptor GPCR family, including the Insulin-Like Peptide 3 INSL3 receptor, is involved in the Nuclear Factor kappa B NF-κB-mediated pathway in inflammation. In this regard, it can be thought that INSL3 plays a role in inflammation via the NF-κB pathway. In this study, we investigated the effect of INSL3 on inflammation and cell viability in the lipopolysaccharide LPS-induced N9 microglia cell line. Materials and Methods: N9 microglial cells were pretreated with INSL3 for 2 hours, and then treated with LPS for 6 hours. Cell viability was identified by WST-8 assay. Immunostaining was performed to evaluate the levels of Interleukin-1β IL-1β, Tumor necrosis factor TNF-α, and NF-κB. Results: The cells in the LPS group showed degenerative changes in morphology and decreased cell viability. In the INSL3LPS group 1.210.06, the general appearance and viability of the cells were more similar to the control group 1.920.04 compared to the LPS group 0.610.05. It was determined that INSL3 prevented the LPS-induced increase in IL-1β, TNF-α, and NF-κB levels and decreased cell death. Conclusion: INSL3 suppresses inflammation and thus promotes cellular healing and can be considered a therapeutic agent that reduces inflammation.

 Purpose: The G-protein coated receptor GPCR family, including the Insulin-Like Peptide 3 INSL3 receptor, is involved in the Nuclear Factor kappa B NF-κB-mediated pathway in inflammation. In this regard, it can be thought that INSL3 plays a role in inflammation via the NF-κB pathway. In this study, we investigated the effect of INSL3 on inflammation and cell viability in the lipopolysaccharide LPS-induced N9 microglia cell line. Materials and Methods: N9 microglial cells were pretreated with INSL3 for 2 hours, and then treated with LPS for 6 hours. Cell viability was identified by WST-8 assay. Immunostaining was performed to evaluate the levels of Interleukin-1β IL-1β, Tumor necrosis factor TNF-α, and NF-κB. Results: The cells in the LPS group showed degenerative changes in morphology and decreased cell viability. In the INSL3LPS group 1.210.06, the general appearance and viability of the cells were more similar to the control group 1.920.04 compared to the LPS group 0.610.05. It was determined that INSL3 prevented the LPS-induced increase in IL-1β, TNF-α, and NF-κB levels and decreased cell death. Conclusion: INSL3 suppresses inflammation and thus promotes cellular healing and can be considered a therapeutic agent that reduces inflammation.

 Amaç: İnsülin Benzeri Peptid 3 INSL3 reseptörünü de içeren G-protein kaplı reseptör GPCR ailesi, inflamasyonda Nükleer Faktör kappa B NF-κB aracılı yolakta yer almaktadır. Bu bakımdan INSL3ün NF-κB yolu üzerinden inflamasyonda rol oynadığı düşünülebilir. Bu çalışmada INSL3ün, lipopolisakkarit LPS ile indüklenen N9 mikroglia hücre hattında inflamasyon ve hücre canlılığı üzerindeki etkisini araştırdık. Gereç ve Yöntem: N9 mikroglial hücreleri, 2 saat boyunca INSL3 ile ön işleme tabi tutuldu, ardından 6 saat boyunca LPS ile işleme tabi tutuldu. Hücre canlılığı WST-8 analizi ile belirlendi. İnterlökin-1β IL-1β, Tümör nekroz faktörü TNF-α ve NF-κB düzeyleri de immünhistokimyasal yöntemlerle değerlendirildi. Bulgular: LPS grubundaki hücrelerde morfolojide dejeneratif değişiklikler ve hücre canlılığında azalma görüldü. INSL3LPS 1.210.06 grubunda hücrelerin genel görünümü ve canlılığı LPS 0.610.05 grubuna göre kontrol grubuna 1.920.04 daha benzerdi. INSL3ün LPS kaynaklı IL-1β, TNF-α ve NF-κB seviyelerindeki artışı önlediği ve hücre ölümünü azalttığı belirlendi. Sonuç: INSL3ün inflamasyonu baskılayarak hücresel iyileşmeyi desteklediği ve inflamasyonu azaltan terapötik bir ajan olarak değerlendirilebileceği sonucuna varıldı.

Makale detayları

INSL3 suppresses LPS-induced inflammation in N9 microglia cells

Yazarlar:

Dilek Şaker | Gülfidan Coşkun | Sait Polat

Yayıncı:

Cukurova University

Ana Başlıklar:

Hücresel İmmünoloji | İmmünoloji (Diğer)

Dergi:

Cukurova Medical Journal Vol.49 Issue 2, pp.489-496

Belge Tipi:

Makale

Yayın Tarihi:

6/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001320801

pISSN:

2602-3032

inflammation

insulin-like peptide 3

lipopolysaccharide

microgliaInflamasyon

insülin benzeri peptid 3

lipopolisakkarit

mikroglia

Sayı

Makale detayları

Yazarlar: Dilek Şaker | Gülfidan Coşkun | Sait Polat

Yayıncı: Cukurova University

Ana Başlıklar: Hücresel İmmünoloji | İmmünoloji (Diğer)

Dergi: Cukurova Medical Journal Vol.49 Issue 2, pp.489-496

Belge Tipi: Makale

Yayın Tarihi: 6/2024

Belge Dili: İngilizce

Document ID (Org No.): 2001320801

pISSN: 2602-3032

Sayı

Yazarlar:

Dilek Şaker | Gülfidan Coşkun | Sait Polat

Yayıncı:

Cukurova University

Ana Başlıklar:

Hücresel İmmünoloji | İmmünoloji (Diğer)

Dergi:

Cukurova Medical Journal Vol.49 Issue 2, pp.489-496

Belge Tipi:

Makale

Yayın Tarihi:

6/2024

Belge Dili:

İngilizce

Document ID (Org No.):

2001320801

pISSN:

2602-3032