Ameliorative Role of Vitamin B Complex in Diclofenac Induced Nephrotoxicity in Rats

Abstract

Diclofenac sodium is a commonly used nonsteroidal anti-inflammatory drug (NSAID) known for its analgesic and anti-inflammatory properties. However, prolonged or high-dose use can harm the kidneys, leading to renal tissue damage. This condition, known as renotoxicity, can adversely affect kidney function. This experimental preclinical in vivo study aimed to investigate the renal tissue damage caused by diclofenac sodium in rats and to evaluate the preventive effects of vitamin B complex. The researchers divided 96 rats into four groups of 24, each with similar weights ranging from 165 to 230 grams. The groups were designated as control, diclofenac sodium, B-complex, and a combination of diclofenac sodium and B-complex. After 14 days, biochemical analyses (including blood urea and serum creatinine levels) and histological examinations (of kidney tissue cross-sections) were performed. The results showed that groups treated with diclofenac sodium had elevated levels of blood urea and serum creatinine, indicating kidney dysfunction. Histological analysis revealed degeneration and congestion in the kidney tissues, pointing to toxicity from diclofenac sodium. In contrast, the B-complex group exhibited nearly normal values for biochemical parameters and maintained healthy kidney tissue, suggesting a protective effect. The adverse effects of diclofenac sodium on the kidneys may be linked to free radicals and mitochondrial dysfunction. Treatment with B-complex reduced oxidative damage and apoptotic cell death associated with diclofenac sodium. In conclusion, diclofenac sodium can lead to renal tissue damage; however, the administration of vitamin B complex seems to mitigate these harmful effects. Further research is needed to explore the underlying mechanisms and establish appropriate clinical dosages.