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Comparative study between effects of ginkgo biloba extract and extract loaded on gold nanoparticles on hepatotoxicity
Amr S Osman1, Sally E Abu-Risha2, Samaa M Bakr3
1Department of Zoology, Faculty of Science, Mansoura University, Mansoura, Egypt.
Abstract:
In human organs, potassium bromate (KBrO3) produces toxicity. The main causes of KBrO3 hepatotoxicity are the formation of reactive oxygen species (ROS) and DNA damage. The purpose of this study is to show how ginkgo biloba extract (GBE) and extract loaded with nanogold particles (GBE@AuNPs) affect hepatotoxicity caused by KBrO3. The rats were separated into eight groups: control (group I), GBE (group II), AuNPs (group III), GBE@AuNPs (group IV), KBrO3 (group V), KBrO3 and GBE (group VI), KBrO3 and AuNPS (group VII), and KBrO3 and GBE@AuNPs (group VIII). KBrO3 generated DNA damage spots in a comet assay, which were associated with increased inflammatory indicators (IL-6), decreased anti-apoptotic Bcl-2, and increased apoptotic markers (Bax and caspase-3). The inflammatory, apoptotic, and ultrastructural alterations in liver tissue produced by KBrO3 were reduced in treated groups VI, VII, or VIII. The hepatotoxic effects of KBrO3 were reduced when GBE, AuNPs, or GBE@AuNPs were used; the particular GBE@AuNPs were the most effective.
Insights
Potassium bromate (KBrO3) causes liver damage via oxidative stress and DNA damage. Ginkgo biloba extract (GBE) and GBE-loaded gold nanoparticles (GBE@AuNPs) protected against KBrO3-induced hepatotoxicity, with GBE@AuNPs showing the highest efficacy.
Area of Science:
- Toxicology
- Hepatology
- Nanotechnology
Background:
- Potassium bromate (KBrO3) is a nephrotoxic and hepatotoxic agent.
- KBrO3-induced liver injury is characterized by oxidative stress, inflammation, and apoptosis.
- Ginkgo biloba extract (GBE) and gold nanoparticles (AuNPs) possess antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the protective effects of GBE and GBE-loaded AuNPs (GBE@AuNPs) against KBrO3-induced hepatotoxicity in rats.
Main Methods:
- Rats were divided into eight groups receiving different treatments: control, GBE, AuNPs, GBE@AuNPs, KBrO3, KBrO3 + GBE, KBrO3 + AuNPs, and KBrO3 + GBE@AuNPs.
- Hepatotoxicity was assessed using comet assay for DNA damage, inflammatory markers (IL-6), and apoptosis markers (Bcl-2, Bax, caspase-3).
- Liver tissue ultrastructure was examined.
Main Results:
- KBrO3 induced significant DNA damage, inflammation, and apoptosis in liver cells.
- Treatment with GBE, AuNPs, or GBE@AuNPs ameliorated KBrO3-induced hepatotoxicity.
- GBE@AuNPs demonstrated the most potent protective effect against KBrO3-induced liver injury.
Conclusions:
- GBE and AuNPs, particularly when combined in GBE@AuNPs, offer significant protection against KBrO3-induced hepatotoxicity.
- The protective mechanisms involve reducing oxidative stress, inflammation, and apoptosis.
- GBE@AuNPs represent a promising therapeutic strategy for mitigating KBrO3-induced liver damage.
