Publication Details
Abstract
Acute kidney injury is among serious drug-induced adverse reactions. Cisplatin is one of the leading drugs causing nephrotoxicity mainly by generating free radicals and inflaming acute tissues. Excessive reactive oxygen species (ROS) production results in disruption of the redox balance, promotes lipid peroxidation, and consumes antioxidant systems like glutathione (GSH). Simultaneously, (SOD). activity decreases. Taken together, all these changes cause the failure of mitochondrial functions, loss of membrane integrity, and induction of proinflammatory pathways like that of B (NF-κB) and tumor necrosis factor-alpha (TNF-α). Besides that, these effects are reflected as histopathological changes, such as inflammatory cell infiltration congestion cellular degeneration and even necrosis in the worst cases. Antioxidants and anti-inflammatory properties are found in a few types of herbs like quercetin and they may have become important agents which reduce the risk of oxidative damage and inflammation, and they help to keep tissue together. This is achieved through boosting our natural ability to fight oxidative stress and altering the body's inflammatory mechanism, this way protecting the cells of the body. Yet, there is not enough clinical evidence to support the use of plants with such properties in all forms of kidney failure at this time, because of this, their usage remains confined to certain clinical support cases. Researches currently are concentrated on examining the protective effects of the natural antioxidant and anti-inflammatory flavonoid, the quercetin, in cisplatin-related severe kidney damage in the rat together with the changes that occur in the rat tissue structure due to this damage. Forty male Wistar rats weighing 200-250 g were randomly divided into four equal groups: a healthy control group, a cisplatin group, a quercetin group, and a cisplatin + quercetin group. Acute injury was induced via a single intraperitoneal injection of cisplatin (6 mg/kg), while quercetin (50 mg/kg) was administered daily for 14 days. After treatment, blood and tissue samples were taken for biochemical and histopathological studies. Measured serum levels of renal function markers included creatinine, urea and total protein, inflammatory mediators were )TNF-α,NF-κB,IL-1β), and antioxidant markers: )GSH,SOD(. All this was backed by histopathological analysis using Hematoxylin and Eosin (H&E) staining of the tissues. Cisplatin-treated animals showed a marked (p < 0.05) increase in the serum levels of creatinine, urea and inflammatory mediators while simultaneously a decrease in serum protein glutathione and superoxide dismutase was observed as evidenced by their blood tests. Their renal tissues, as examined microscopically, showed severe damage in tubular cells. Administration of queringetin with quite successfully reversed some of the pathological and biomorphological changes observed in cisplatin-treated group. The study concludes that quercetin offers a protective role against cisplatininduced nephrotoxicity and this may be due to the antioxidant and anti-inflammatory features of the compound.