Effects of Bee Venom on Cadmium Toxicity in Albino Rats
Effects of Bee Venom on Cadmium Toxicity in Albino Rats
Mariam Ismail Ali1*, Rania Helmi Abdou1, Mary Ayad Sargious2, Omnia Mohamed Khattab2, Kawthar Abdelwahed Elhady1
ABSTRACT
The present study aimed to confirm the mitigation effects of bee venom at a dose of 2mg/kg against cadmium chloride hepatotoxicity, nephrotoxicity, and neurotoxicity in rats. The study found that cadmium treatment in rats increased inflammatory markers (TNF-α 264.3% and IL-1β 170.7%), and oxidative markers(MDA 140.5%), Higher liver enzymes, histopathological lesions, and genes expression screened for hepatotoxic effects. Bee venom effectively reduced inflammation (TNF-α 49% and IL-1β 41.4%) and oxidation (MDA 36.8%), reduced liver enzymes, and enhanced histopathologic lesions with score 1, as confirmed by the difference in regulation of inflammatory genes (TNF-α 37% increase, IL-1β 15% reduction, and NF-kB19% reduction) and massive increase of pro-apoptotic Bax in the liver. Not only the potential beneficial role of bee venom on cadmium hepatotoxic effects but also nephrotoxic and neurotoxic effects and reducing hepatotoxicity caused by cadmium exposure via regulating, Bax, and NF-kB signaling pathways in rats by considering its possible antioxidant, anti-inflammatory, and anti-apoptotic effects. The results showed the nephrotoxic effect of cadmium: a significant increase in serum creatinine, urea, and histopathological lesions in the kidney of cd-treated rats. Bee venom showed nephroprotective effects, decreasing serum creatinine and urea by 16.9% and73.4% respectively and also improving histopathologic lesions in the kidney. Also, the neuroprotective effect of bee venom appeared in the improvement of the histopathological lesions in the brain.
Keywords: Cadmium, Bee venom, Oxidative stress, Inflammation, Apoptosis
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October 2024
Vol. 12, Sp. Iss. 1
