Scientific African (Dec 2024)
Improvement in kidney damage resulting from stanozolol intramuscular injections in rats by Natural Cocoa Powder (NCP) administration
Abstract
Background: Stanozolol, an anabolic steroid, has been shown to induce kidney damage through mechanisms involving oxidative stress and inflammation. Natural Cocoa Powder (NCP), known for its high antioxidant content, may offer protective effects against such damage. Aim: This study aimed to evaluate the potential of Natural Cocoa Powder (NCP) in ameliorating kidney damage caused by stanozolol intramuscular injections in rats. Methods: Thirty rats were randomly assigned into five groups (G1–G5) and fed with standard rat chow. G1 and G3 received 2 mg/kg stanozolol intramuscularly twice weekly, G2 and G4 received 5 mg/kg stanozolol twice weekly, while G5 served as the control with no stanozolol. G1, G2, and G5 had 24 h access to water, while G3 and G4 had water replaced with 2 % NCP from 6 am to 6 pm daily. After 8 weeks, kidneys were perfusion-fixed and analyzed histomorphometrically for proximal/distal tubules, Bowman's space, glomerular tuft, and renal corpuscle composition.Before and after treatments, renal function was measured by serum creatinine and blood urea nitrogen, whilst systemic inflammation was monitored by erythrocyte sedimentation rate and serum C-reactive protein tests. Results and Discussion: Stanozolol administration significantly increased kidney damage in a dose-dependent manner, with marked rises in the volume densities of the proximal convoluted tubule (PCT), distal convoluted tubule (DCT), glomerular tuft, and renal corpuscle. At higher doses, PCT and DCT volume densities increased by 143 % and 223 %, respectively, compared to controls. Natural cocoa powder (NCP) mitigated these effects, reducing PCT, DCT, and glomerular tuft volume densities by 92 %, 77 %, and 86 %, respectively. Stanozolol also elevated serum markers of kidney dysfunction and inflammation, such as blood urea nitrogen (BUN), serum creatinine (SCr), and C-reactive protein (CRP). While NCP significantly lowered BUN and SCr levels, it did not fully normalize CRP, which remained elevated in stanozolol-treated rats. Conclusion: Increased volume density of kidney components indicated hypertrophy, which was associated with elevated serum creatinine, blood urea nitrogen (BUN), and C-reactive protein (CRP) levels, reflecting impaired renal function and heightened systemic inflammation. The reduction in these markers with NCP ingestion suggests its potential to mitigate stanozolol-induced renal damage. It is proposed that the antioxidant properties of NCP may have reduced inflammation by counteracting oxidative stress, thereby contributing to the observed improvement in kidney function and structure.
