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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
ROLE OF DIMETHYL FUMARATE (NRF2 ACTIVATOR) IN REDUCING OF CIPROFLOXACIN-INDUCED HEPATOTOXICITY IN RATS VIA THE
Mahmood Jawad1, Karam Al-Akkam2, Manar Mohammed3
1AL-ZAHRAWI UNIVERSITY COLLEGE, KARBALA, IRAQ.
Objective:
The aim: The present study aims to study the effect of DMF on ciprofloxacin-induced liver damage as assessed by liver function and liver pathology and to study this effect if it is thought to activate the Nrf2 antioxidant defense mechanism.
Patients And Methods:
Materials and methods: G1 (control), G2 (ciprofloxacin group), G3 and G4 (two DMF groups rats treated with DMF 50mg and 100mg), and G5 and G6 (two DMF groups rats treated with DMF 50mg and 100mg) (two ciprofloxacin Plus DMF at 50 mg and 100 mg). The tests included study of liver function, Nrf2 analysis, and anti-oxidant enzyme analysis.
Results:
Results: The serum blood Nrf2, HO-1, and tissue anti-oxidant enzymes all increased after ciprofloxacin treatment. The serum levels of Nrf2 and HO-1 were higher in the ciprofloxacin plus DMF groups, but anti-oxidant enzymes were lower. DMF increased Nrf2 expression in rats when ciprofloxacin caused hepatotoxicity.
Conclusion:
Conclusions: DMF lowers experimental hepatotoxicity in vivo. This effect is thought to activate the Nrf2 antioxidant defense mechanism.
Insights
Dimethylformamide (DMF) reduces liver damage caused by ciprofloxacin in rats. This protective effect is linked to the activation of the Nrf2 antioxidant pathway, suggesting a potential therapeutic mechanism.
Area of Science:
- Pharmacology
- Toxicology
- Biochemistry
Background:
- Ciprofloxacin can induce liver damage (hepatotoxicity).
- The Nrf2 pathway is a key cellular defense against oxidative stress.
- Dimethylformamide (DMF) is being investigated for potential protective effects.
Purpose of the Study:
- To evaluate the effect of DMF on ciprofloxacin-induced liver injury.
- To determine if DMF activates the Nrf2 antioxidant defense mechanism in this context.
Main Methods:
- Animal model using rats divided into control, ciprofloxacin, and ciprofloxacin plus DMF groups.
- Assessment of liver function and pathology.
- Analysis of Nrf2 and antioxidant enzyme levels (e.g., HO-1).
Main Results:
- Ciprofloxacin treatment increased markers of liver damage and Nrf2/HO-1 levels.
- Co-administration of DMF with ciprofloxacin further elevated serum Nrf2 and HO-1.
- DMF treatment enhanced Nrf2 expression in the context of ciprofloxacin-induced hepatotoxicity.
Conclusions:
- DMF demonstrates a protective effect against experimental hepatotoxicity in vivo.
- Activation of the Nrf2 antioxidant defense mechanism is a likely contributor to DMF's protective action.
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