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Reno-protective effect of berberine.
Nawar Raad Hussien1, Hayder M Al-Kuraishy1, Ali Ismail Al-Gareeb1
1Department of Clinical Pharmacology, Medicine and Therapeutic, Al- Mustansiriya University, Baghdad, Iraq.
Berberine effectively protected against diclofenac-induced acute kidney injury in rats. It reduced kidney damage markers and enhanced antioxidant capacity, showing reno-protective potential.
Area of Science:
- Pharmacology
- Toxicology
- Nephrology
Background:
- Diclofenac, a non-steroidal anti-inflammatory drug, can cause acute kidney injury.
- Oxidative stress and inflammation are key mechanisms in drug-induced nephrotoxicity.
- Berberine is a natural compound with known antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the renoprotective effects of berberine against diclofenac-induced acute kidney injury in a rat model.
- To evaluate the impact of berberine on oxidative stress and inflammatory biomarkers in the kidneys.
Main Methods:
- Male Sprague Dawley rats were divided into three groups: control, diclofenac-induced injury, and berberine plus diclofenac treatment.
- Kidney function markers (blood urea, serum creatinine), oxidative stress markers (malondialdehyde, superoxide dismutase, glutathione reductase), and kidney injury biomarkers (NGAL, KIM-1, IL-18, cystatin-c) were measured.
- Statistical analysis was performed using SPSS 20.
Main Results:
- Berberine significantly reduced levels of blood urea, serum creatinine, malondialdehyde, NGAL, KIM-1, and IL-18 compared to the diclofenac-only group.
- Berberine treatment led to a significant increase in superoxide dismutase and glutathione reductase levels, indicating improved antioxidant capacity.
- The study demonstrated berberine's ability to attenuate kidney damage markers.
Conclusions:
- Berberine exhibits significant renoprotective effects against diclofenac-induced acute kidney injury in rats.
- Berberine acts by modulating pro-inflammatory and oxidative stress biomarkers.
- These findings suggest berberine as a potential therapeutic agent for mitigating NSAID-induced nephrotoxicity.
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