Answers are grounded in this paper and cite their sources.
This study investigated the protective effect of alkaloid boldine against diclofenac-induced kidney damage in normotensive female rats. 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. 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. 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.
No takes yet. Share an insight, caveat, or question.
Cristofolini et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: