DMF Attenuates Ciprofloxacin-lnduced Nephropathy in Rats via Nrf2 Pathway

Saif M. Hassan, Raid M. Al Abood, Mohammed Jasim Jawad, Mahmood J. Jawad, Nagham Al-Zubidi

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Background: The pathophysiology of ciprofloxacin-induced nephropathy (CIN) is complicated by oxidative stress. The goal of this study was to see if Dimethyl Fumarate (DMF) has any antioxidant properties in a rat model of CIN. Methods: Rats were randomly assigned to six groups (n=8): control, ciprofloxacin (ciprofloxacin-induced CIS), two DMF groups (rats treated with DMF 50mg and lOOmg), and two ciprofloxacin Plus DMF groups (n=8 group) (CDC rats treated with DMF at 50 mg and 100 mg). Renal function testing, Nrf2 analysis, and anti-oxidant enzymes analysis was all done. Results: Following ciprofloxacin therapy serum blood urea nitrogen (BUN), creatinine, and anti-oxidant enzymes all rose. In the ciprofloxacin - DMF groups, serum BUN and creatinine were lower, and anti-oxidant enzymes were higher than in the ciprofloxacin group, in CIN rats, DMF upregulated Nrf2 expression. Conclusions: In vivo, DMF reduces experimental CIN. It's thought that this impact activates the Nrf2 antioxidant defenses pathway.

Original languageEnglish (US)
Pages (from-to)87-91
Number of pages5
JournalJournal of Pharmaceutical Negative Results
Issue number2
StatePublished - 2022


  • Anti-oxidants
  • Ciprofloxacin
  • Creatinine
  • Nrf2
  • Urea

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science
  • Drug Discovery


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