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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.
Insights
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.
Objective:
To assess the reno-protective effect of berberine on diclofenac-induced acute kidney injury in rats.
Methods:
The experimental study was conducted at the College of Medicine, Mustansiriya University, Baghdad, Iraq, from January to March 2018, and comprised Sprague Dawley male rats which were divided into 3 equal groups. Group1 rats were treated with distilled water plus normal saline for 14 days, Group2 rats were treated with distilled water plus diclofenac for 14 days and Group3 rats were treated with berberine plus diclofenac for 14 days. Parameters measured were blood urea, serum creatinine, serum malondialdehyde, superoxide dismutase, glutathione reductase, neutrophil gelatinase associated lipocalin, kidney injury molecules-1, Interleukin-18and cystatin-c. Anthropometric measurements and estimated glomerular filtration rate were also noted. SPSS 20 was used for data analysis.
Results:
Of the 30 rats, the three groups had 10(33.3%) each. Berberine reduced blood urea, serum creatinine, malondialdehyde, neutrophil gelatinase associated lipocalin, kidney injury molecules-1 and Interleukin-18 significantly compared to diclofenac-induced acute kidney injury (p<0.01 each). Berberine improved anti-oxidant capacity through significant elevation of superoxide dismutase and glutathione reductase sera levels (p<0.01 each).
Conclusions:
Berberine was found to be an effective agent in the attenuation of diclofenac-induced acute kidney injury through the modulation of pro-inflammatory and oxidative stress biomarkers.
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