Protective effect of Vitex negundo L. in diclofenac induced nephrotoxicity

Abstract

Major morbidity and mortality are related to kidney damage, a complex clinical disease. About 19–33% of hospitalized patients' AKI episodes are caused by drug-induced nephrotoxicity.Non-steroidal anti-inflammatory medications, like diclofenac, are thought to be safe, but in recent years, they have drawn particular attention because of the possibility of kidney damage.Vitex negundo, or nigundi, has anti-inflammatory qualities. In this study, we looked into how well Nirgundi (Vitex negundo) worked to prevent Wistar rats from developing nephrotoxicity from diclofenac. After a 7 day intramuscular course of diclofenac 10 mg per kg b/w, we found that it increased in urea, creatinine, electrolytes (potassium, sodium, and chloride), and decreased urine output.Furthermore, diclofenac caused morphological alterations that were consistent with renal injury and elevated oxidative stress in renal tissue (raising MDA levels and decreasing SOD levels). However, Vitex negundo decreased creatinine, blood urea, and electrolytes brought on by diclofenac while also boosting urine production. Vitex negundo, prevented the kidneys from producing cytokines, oxidative stress, morphological alterations, and apoptosis when exposed to diclofenac. Vitex negundo, is effective in preventing nephrotoxicity caused by diclofenac sodium.