The investigation of protective effect of punicalagin on cisplatin-induced kidney damage

The aim of this study was to investigate the protective effect of punicalagin against cisplatin-induced renal injury. In this study, 32 BALB/c breed male/female mice (8 week old ) were divided into 4 groups. Group 1 served as control and received saline solution intraperitoneally (i.p.) for 3 days. Group 2 (punicalagin group) mice received punicalagin 15 mg/kg for 3 days, i.p. Group 3 (Cisplatin group) mice received a single dose of 20 mg/kg cisplatin i.p. Group 4 mice (punicalagin+cisplatin group) were given a single dose of cisplatin (20 mg/kg i.p.) and punicalagin (15 mg/kg i.p. s.i.d.) for 3 days. At the end of the study, serum urea, creatinine, total oxidant and total antioxidant status (TOS and TAS), renal tissue TAS and TOS levels were determined. In addition, hematoxylin-eosin staining was performed histopathologically and immunohistochemically Bcl-2, TNFα, NF-кB were evaluated for renal changes. At the end of the experiment, urea levels in the cisplatin group increased significantly compared to the control and punicalagin groups (p <0.05). In contrast, urea level in punicalagin + cisplatin group was lower than cisplatin group. Urea levels were higher than control and punicalagin groups. Serum creatinine level increased in the cisplatin group compared to the control group (p <0.05), while the creatinine level in the punicalagin + cisplatin group did not differ compared to the control group (p> 0.05). Serum and renal tissue TAS levels of cisplatin group decreased significantly compared to control group, while TOS levels increased significantly (p <0.05). The serum and renal tissue TAS and TOS levels of the punicalagin+cisplatin group did not differ from the control group (p> 0.05). Histopathologic examination revealed severe hyperemia in cisplatin group, protein fluid accumulation in lumens of tubules and sclerosis in glomeruli. In the punicalagin+cisplatin group, these findings decreased significantly. When Bcl-2 expressions of kidneys were examined, negative reaction was observed in control and punicalagin groups, whereas significantly increased immunoreaction in both tubular epithelium and glomeruli in ciplatin group. In the punicalagin+cisplatin group, the immune reaction was significantly reduced compared to the cisplatin group. When NF-kB and TNF-α immunoreaction were examined in the kidneys, negative expression was observed in the control and punicalagin group, whereas intensive expression was observed in multiple cells and renal tubular epithelium in the ciplatin group, respectively. The immunoreactivity was decreased in the punicalagin + cisplatin group compared to the cisplatin group. As a result, according to biochemical and histopathological findings, it was concluded that punicalalgin has protective effect against cisplatin induced kidney damage and oxidative stres, and punicalalgin could be used as a protective and therapeutic agent during cisplatin treatment. Keywords: Cisplatin, Punicalagin, Kidney damage, Protective effect