Abstract
Objective
This study investigated the protective effect of alkaloid boldine against
diclofenac-induced kidney damage in normotensive female rats.
Methods
Animals were divided into three groups: naive, vehicle+diclofenac (50 mg/kg),
and boldine+diclofenac (boldine 0.1 mg/kg+diclofenac 50 mg/kg). Treatments
were administered orally once daily for 2 days.
Results
The vehicle+diclofenac group showed reduced urinary volume and sodium
excretion. In contrast, the boldine+diclofenac group restored both
parameters to levels similar to the naive group. Other urinary electrolytes
indicated imbalance in diclofenac-treated animals, regardless of boldine
co-treatment. Plasma analysis showed no alterations. Kidney tissue from
diclofenac-treated groups revealed increased glutathione and decreased lipid
hydroperoxides. Histology showed that vehicle+diclofenac resulted in a
reduction in glomerular size, thickening of Bowman’s capsule, and mesangial
disarray, while these changes were less pronounced with boldine
co-treatment. Molecular docking analysis indicated that boldine may interact
with important proteins related to renal hemodynamics, sodium regulation,
and inflammatory processes pointing to a multi-target mechanism.
Conclusions
Boldine attenuated renal damage induced by diclofenac, improving urinary
parameters and reducing histological alterations. Further studies are
necessary to elucidate its protective mechanisms and impact on renal
hemodynamics.
Keywords
non-steroidal anti-inflammatory - electrolytes - kidney - oxidative stress