Allicin ameliorates kidney function and urinary bladder sensitivity in cyclosporine A-treated rats

Area of Science:

• Pharmacology
• Nephrology
• Toxicology

Background:

• Cyclosporine-A (CsA) is a vital immunosuppressant for organ transplantation and autoimmune diseases.
• CsA's therapeutic use is significantly limited by its dose-dependent nephrotoxicity.
• Oxidative stress and inflammation are key mechanisms in CsA-induced kidney damage.

Purpose of the Study:

• To investigate the protective effect of allicin against CsA-induced nephrotoxicity in a rat model.
• To evaluate allicin's impact on CsA-induced oxidative stress and inflammation in kidney tissue.
• To assess allicin's influence on CsA-induced changes in urinary bladder sensitivity to acetylcholine (ACh).

Main Methods:

• Rats were divided into control, CsA-treated, and CsA/allicin-treated groups.
• Kidney function was assessed via serum creatinine, blood urea nitrogen, and urinary protein levels.
• Renal oxidative stress markers (malondialdehyde, glutathione, nitric oxide) and inflammatory markers (TNF-α, MPO) were measured.
• Histopathological examination of kidney tissues and in vitro assessment of urinary bladder ring sensitivity to ACh were performed.

Main Results:

• CsA administration significantly increased kidney/body weight ratio, serum creatinine, BUN, and urinary protein, indicative of nephrotoxicity.
• CsA induced significant renal oxidative stress and inflammation, evidenced by altered MDA, GSH, NOx, TNF-α, and MPO levels.
• CsA exposure increased urinary bladder ring sensitivity to ACh, while allicin treatment ameliorated these effects.
• Histological analysis confirmed CsA-induced tubular necrosis and atrophy, which were attenuated by allicin.

Conclusions:

• Allicin demonstrates significant protective effects against CsA-induced nephrotoxicity in rats.
• Allicin mitigates CsA-induced renal injury by reducing oxidative stress, inflammation, and restoring nitric oxide levels.
• Allicin may be a potential therapeutic agent to prevent or reduce CsA-related kidney damage and associated bladder hypersensitivity.