What type of study is this?

This is a In Vitro Study study.

What question did this study set out to answer?

This study aims to evaluate the protective effects of bee pollen and bee pollen-loaded SLNs against lead acetate-induced nephrotoxicity.

March 22, 2026

Comparison of Protective Effects of Bee Pollen and Bee Pollen-Loaded Solid Lipid Nanoparticles Against Lead Acetate-Induced Nephrotoxicity: In Vitro and In Vivo Model

Key Points

This study aims to evaluate the protective effects of bee pollen and bee pollen-loaded SLNs against lead acetate-induced nephrotoxicity.
Forty adult male Wistar rats were randomly divided into eight groups
Rats received treatments with lead acetate and various doses of bee pollen or SLNs for 14 days
Biochemical and histopathological assessments were performed to evaluate renal injury.
Lead acetate significantly increased serum levels of urea, total bilirubin, and oxidative stress markers
Bee pollen, especially the SLNs, restored these biochemical parameters and reduced oxidative stress
Treatment with bee pollen improved antioxidant enzyme activities and histopathological alterations in kidney tissue.

Abstract

Introduction: The kidney is one of the most susceptible organs to lead toxicity. In this study, we evaluated the protective and ameliorative effects of bee pollen and bee pollen-loaded Solid Lipid Nanoparticles (SLNs) against lead acetate-induced renal injury in adult male rats. Methods: Forty adult male albino Wistar rats were randomly divided into eight groups (n=5 per group): a control group (4 ml/kg olive oil), a lead acetate group (25 mg/kg), three groups treated with lead acetate (25 mg/kg) plus bee pollen extract at doses of 200, 400, and 800 mg/kg, and three groups treated with lead acetate (25 mg/kg) plus bee pollen-loaded SLNs at the same doses, administered for 14 consecutive days. Results: Lead acetate significantly increased serum uric acid, creatinine, urea, and total bilirubin levels; elevated renal tissue Malondialdehyde (MDA) and Nitric Oxide (NO) levels; reduced total thiol content, Glutathione (GSH), and Total Antioxidant Capacity (TAC); and decreased the activity of antioxidant enzymes Catalase (CAT), Superoxide Dismutase (SOD), and Glutathione Peroxidase (GPX) in kidney tissue. Supplementation with bee pollen, particularly bee pollen SLNs, restored serum biochemical parameters and attenuated oxidative stress markers in renal tissue. Moreover, it enhanced kidney GSH, total thiol, and TAC levels, increased antioxidant enzyme activities, and significantly improved lead-induced histopathological alterations. Lead acetate exposure also decreased the viability of Artemia salina larvae and HEK293 cells, effects that were markedly reversed by bee pollen and especially by bee pollen SLN treatment. Discussion: Lead acetate intoxication significantly increased serum biochemical parameters and oxidative markers and diminished total thiol, TAC, GSH, and antioxidant enzymes. Additionally, histological findings signified that lead exposure has substantial destructive effects on kidney tissue. Meanwhile, treatment with bee pollen extract and bee pollen SLNs remarkably reversed serum biochemical and oxidative markers, restored total thiol, TAC, GSH, and antioxidant enzymes, and improved kidney histological alterations. In this regard, bee pollen SLN has more outstanding ameliorative features that could be ascribed to the application of SLN formulation toward improvement in physicochemical properties of bee pollen extract. Conclusion: These results demonstrate that bee pollen, especially in nanoform, exerts protective effects against lead-induced nephrotoxicity both in vitro and in vivo, suggesting its potential as a therapeutic agent against lead poisoning.

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