title: Anti-oxidant and anti-inflammatory effects of apigenin in a rat model of sepsis: an immunological, biochemical, and histopathological study.
abstract: OBJECTIVE
  We hypothesize that apigenin may inhibit some cellular process of sepsis-induced spleen injury and simultaneously improve inflammation and oxidative stress. Therefore, the aim of this study was to investigate the potential protective effects of apigenin in a polymicrobial sepsis rat model of by cecal ligation and puncture.
  
  
  METHODS
  64 female Wistar albino rats were divided into 8 groups. The pro-inflammatory (tumor necrosis factor-alpha, interleukin-6, and interleukin-1-beta) and anti-inflammatory (tumor growth factor-beta and interleukin-10) cytokine levels were measured by enzyme-linked immunosorbent assay. CD3, CD68, and nuclear factor kappa B (NF-κB) positivity rates were detected by immunohistochemical methods. Oxidative stress parameters were measured by tissue biochemistry.
  
  
  RESULTS
  Sepsis caused a significant increase in TNF-alpha, IL-1-beta, IL-6, and TGF-beta levels whereas it reduced IL-10 level. Additionally, it led to an increase in CD3, CD68, and NF-κB positivity rates as well as oxidative stress parameters levels. However, apigenin inhibited the inflammation process, increased the IL-10 level and normalized the oxidative stress parameters.
  
  
  CONCLUSIONS
  Pretreatment with apigenin results in a significant reduction in the amount of inflammatory cells. The beneficial effect of apigenin on spleen injury also involved inhibition of NF-κB pathway, suppression of proinflammatory cytokines, and induction of anti-inflammatory cytokine production. Additionally, it led to a decrease in oxidative stress in spleen tissue. Taking everything into account, apigenin may be an alternative therapeutic option for prevention of sepsis-induced organ.
authors.affiliation: a Department of Microbiology, Faculty of Medicine , Kafkas University , Kars , Turkey ;
authors.forename: Murat
authors.initials: M
authors.lastname: Karamese
authors.affiliation: b Department of Biochemistry, Faculty of Veterinary Medicine , Ataturk University , Erzurum , Turkey ;
authors.forename: Huseyin Serkan
authors.initials: HS
authors.lastname: Erol
authors.affiliation: c Department of Pathology, Faculty of Medicine , Ataturk University , Erzurum , Turkey ;
authors.forename: Mevlut
authors.initials: M
authors.lastname: Albayrak
authors.affiliation: d Department of Pathology, Faculty of Medicine , Kafkas University , Kars , Turkey ;
authors.forename: Gulname
authors.initials: G
authors.lastname: Findik Guvendi
authors.affiliation: e Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine , Kafkas University , Kars , Turkey ;
authors.forename: Emsal
authors.initials: E
authors.lastname: Aydin
authors.affiliation: f Department of Histology and Embryology, Faculty of Medicine , Kafkas University , Kars , Turkey.
authors.forename: Selina
authors.initials: S
authors.lastname: Aksak Karamese
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D047310:Apigenin / Q000494:pharmacology*; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D005260:Female; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000188:drug therapy* / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D016207:Cytokines; D047310:Apigenin
keywords: Apigenin; CD3 and CD68; CLP sepsis; NF-κB; cytokines; oxidative stress