Abstract

Aim: The goal of this experiment was to examine if Clopidogrel might protect the lungs during sepsis by modulating the inflammatory and oxidative stress markers. Materials and Methods: Twenty-four adult male Swiss-albino mice aged 8-12 weeks, with a weighing of 20-30 g, were randomized into 4 equal groups (n=6): sham (Laparotomy without cecal ligation and puncture [CLP]), CLP (laparotomy plus CLP), vehicle (DMSO 1 hour prior to CLP), Clopidogrel (50 mg/g IP 1 hour before to CLP). ELISA was used to assess Lung tissue levels of pro-inflammatory and oxidative stress markers. Results: F2 isoprostane levels were significantly higher in the sepsis group (p<0.05) in comparison with sham group, while Clopidogrel was considerably lower (p<0.05) in the inflammatory and oxidative stress markers in comparison to sepsis group. Histologically, all mice in the sepsis group had considerable (p=0.05) lung tissue damage, but Clopidogrel considerably decreased lung tissue injury (p=0.05). Conclusion: Clopidogrel was found to reduce lung tissue cytokine concentrations (IL-1, TNF a, IL-6, F2 isoprostane, GPR 17, MIF) in male mice during CLP-induced polymicrobial sepsis by modulation of pro-inflammatory and oxidative stress cascade signaling pathways, to the best of our abilities, no study has looked at the effect of Clopidogrel on MIF levels.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call