Oleuropein Has Modulatory Effects on Systemic Lipopolysaccharide-Induced Neuroinflammation in Male Rats


Şahin S., Şahin E., Esenülkü G., Renda G., Gürgen S. G., Alver A., ...Daha Fazla

JOURNAL OF NUTRITION, cilt.154, sa.4, ss.1282-1297, 2024 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 154 Sayı: 4
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1016/j.tjnut.2024.02.017
  • Dergi Adı: JOURNAL OF NUTRITION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, Agricultural & Environmental Science Database, Applied Science & Technology Source, Art Source, BIOSIS, CAB Abstracts, Chemical Abstracts Core, CINAHL, Environment Index, Food Science & Technology Abstracts, Gender Studies Database, Public Affairs Index, SportDiscus, Veterinary Science Database
  • Sayfa Sayıları: ss.1282-1297
  • Anahtar Kelimeler: astrocyte, IL-17A, IL-4, neuroinflammation, oleuropein
  • Karadeniz Teknik Üniversitesi Adresli: Evet

Özet

Background: Neuroin fl ammation induced by systemic in fl ammation is a risk factor for developing chronic neurologic disorders. Oleuropein (OLE) has antioxidant and anti-in fl ammatory properties; however, its effect on systemic in fl ammation-related neuroin fl ammation is unknown. Objectives: This study aimed to determine whether OLE protects against systemic lipopolysaccharide (LPS)-induced neuroin fl ammation in rats. Methods: Six-wk-old Wistar rats were randomly assigned to 1 of the following 5 groups: 1 ) control, 2 ) OLE-only, 3 ) LPS & thorn; vehicle, 4 ) OLE & thorn; LPS (O-LPS), and 5 ) a single-dose OLE & thorn; LPS (SO-LPS group). OLE 200 mg/kg or saline as a vehicle was administered via gavage for 7 d. On the seventh day, 2.5 mg/kg LPS was intraperitoneally administered. The rats were decapitated after 24 h of LPS treatment, and serum collection and tissue dissection were performed. The study assessed astrocyte and microglial activation using glial fi brillary acidic protein (GFAP) and CD11b immunohistochemistry, nod -like receptor protein -3, interleukin (IL)-1 beta , IL -17A, and IL -4 concentrations in prefrontal and hippocampal tissues via enzyme-linked immunosorbent assay, and total antioxidant/oxidant status (TAS/TOS) in serum and tissues via spectrophotometry. Results: In both the O-LPS and SO-LPS groups, LPS-related activation of microglia and astrocytes was suppressed in the cortex and hippocampus ( P < 0.001), excluding cortical astrocyte activation, which was suppressed only in the SO-LPS group ( P < 0.001). Hippocampal GFAP immunoreactivity and IL -17A concentrations in the dentate gyrus were higher in the OLE group than those in the control group, but LPS-related increases in these concentrations were suppressed in the O-LPS group. The O-LPS group had higher cortical TAS and IL -4 concentrations. Conclusions: OLE suppressed LPS-related astrocyte and microglial activation in the hippocampus and cortex. The OLE-induced increase in cortical IL -4 concentrations indicates the induction of an anti-in fl ammatory phenotype of microglia. OLE may also modulate astrocyte and IL -17A functions, which could explain its opposing effects on hippocampal GFAP immunoreactivity and IL -17A concentrations when administered with or without LPS.