Low concentration of oleic acid exacerbates LPS-induced cell death and inflammation in human alveolar epithelial cells


KÜÇÜKGÜL A., ERDOGAN S.

Experimental Lung Research, cilt.43, sa.1, ss.1-7, 2017 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 43 Sayı: 1
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1080/01902148.2016.1267823
  • Dergi Adı: Experimental Lung Research
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1-7
  • Anahtar Kelimeler: apoptosis, inflammation, lipopolysaccharide, lung injury, oleic acid
  • Hatay Mustafa Kemal Üniversitesi Adresli: Evet

Özet

Purpose: The current study aimed to investigate in vitro effects of oleic acid on lipopolysaccharide (LPS)-induced acute lung injury in the human lung epithelial cells (A549). Materials and Methods: The cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) tests. Selected gene expression levels were analyzed by Real-Time Quantitative-Polymerase Chain Reaction (RT-qPCR). Results: 24 hours of LPS (100 ng/mL) exposure decreased the cells’ viability by 44.6% compared to untreated control. Low concentration (2.5 nM) of oleic acid slightly suppressed the cell survival by 9.1% analyzed 24 hours after incubation. However, oleic acid pretreatment before LPS exposure significantly increased cell survival loss to 63.9%. LPS exposure decreased the expressions of catalase (CAT) and glutathione peroxidase (GPx) mRNA levels by 2.8 and 2.5 fold, respectively. Moreover, pretreatment of the cells with oleic acid strengthened LPS-decreased expressions of CAT and GPx genes by 3.5 and 6.7 fold, respectively. The mRNA expressions of superoxide dismutase (SOD), induced nitric oxide synthase (iNOS), interleukin-1β, IL-12, COX-2, caspase-3 and caspase-8 were increased by 2.4, 2.2, 2.2, 2.3, 3.0, 2.6, and 2.5 fold, respectively, by LPS, and oleic acid pretreatment significantly potentiated the effect of LPS. Conclusion: Oleic acid worsens LPS-induced cell death by potentiating oxidative stress and inflammation in A549 lung epithelial cells.