Abstract
Cadmium exposure induces nephrotoxicity by mediating oxidative stress, inflammation, and apoptosis. The purpose of this study was to examine the protective effect of royal jelly on Cd-induced nephrotoxicity. Adult male mice were distributed randomly into 4 clusters: untreated, royal jelly-treated (85 mg/kg, oral), CdCl2-treated (6.5 mg/kg, intraperitoneal), and pretreated with royal jelly (85 mg/kg) 2 h before CdCl2 injection (6.5 mg/kg, intraperitoneal) for seven consecutive days. Cd concentration in the renal tissue and absolute kidney weight of the Cd-treated mice were significantly higher than those of control group. The levels of kidney function markers, kidney injury molecules-1 (KIM-1), metallothionein, lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1β, and the apoptosis regulators Bax and caspases-3 also increased significantly in the renal tissue of Cd-treated mice, whereas the levels of glutathione, antioxidant enzyme activities, and the apoptosis inhibitor Bcl-2 were significantly reduced in the renal tissue of Cd-treated group. Histopathological studies showed vacuolation and congested glomeruli in the kidney tissue of Cd-treated mice. However, all aforementioned Cd-induced changes were attenuated by pretreatment with royal jelly. We therefore concluded that royal jelly attenuated Cd-induced nephrotoxicity and it is suggested that this nephroprotective effect could be linked to its ability to promote the nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.
Highlights
Cadmium is a reactive metal which negatively affects mammalian organs, such as the brain, liver, kidney, placenta, and testis[1,2]
Mice intoxicated with Cd showed some clinical signs of cadmium toxicity including inappetence, increase in urination, slight decrease of the body weight and increase in respiratory
royal jelly (RJ) pretreatment abrogated all of those deterioration effects of Cd, as suggested by the significant decrease in Cd concentration, level of kidney function markers, and kidney weight compared with those of CdCl2-treated mice
Summary
Cadmium is a reactive metal which negatively affects mammalian organs, such as the brain, liver, kidney, placenta, and testis[1,2]. Occupational and environmental exposure to cadmium cause severe degeneration to the kidney. Cadmium may induce nephrotoxicity by generating reactive oxygen species (ROS), inflammation, and apoptosis in the kidney tissue[1,6]. Elkhadragy et al.[2] reported that S1 and S2 segments of the proximal tubules are the main target site of cadmium nephrotoxicity. It is important to counter the cadmium toxicity-induced generation of free with natural antioxidants, as synthetic chelating agents have showed several undesirable side effects. This study aimed to explore the nephroprotective activity of royal jelly (RJ) against CdCl2-induced nephrotoxicity in male mice
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