Investigation of the Effect of Chloroquine on Adriamcycin-Induced Kidney Damage

Abstract

Although Adriamycin (ADR) is an important anticancer drug used in chemotherapy, it causes nephrotoxicity. The inflammation pathway has an important role in ADR-induced nephrotoxicity. Chloroquine (CLQ), which is used as an antimalarial drug, is used in many diseases. Also, CLQ is known as an anti-inflammatory. In this study, we aimed to investigate the effect of CLQ against nephrotoxicity caused by ADR through the inflammatory pathway. Groups were formed as follows; Control (n = 8), CLQ (n = 8) 50 mg / kg intraperitoneally (i.p.) per day, ADR (n = 8) 2 mg / kg i.p. every 3 days, ADR + CLQ (n = 8) 2mg / kg / i.p. ADR + 50 mg / kg / i.p. CLQ. The experiment took a total of 30 days. At the end of the experiment, kidney tissues were taken from the rats under anesthesia. After fixation in the removed kidney tissues, the tissues were embedded in paraffin by histological methods. Sections were taken from kidney tissues. Renal tissue histopathology and Tumor necrosis factor-alpha (TNF-?) and Nuclear factor-?B p65 (NF-?B p65) immunoreactivities were evaluated. When the kidney tissue was examined, it was seen that damage was caused by ADR. In addition, it was observed that TNF-? and NF-?B p65 immunoreactivities in the kidney significantly increased in the ADR group (p<0.05). Damage and inflammatory markers were found to be decreased in the ADR + CLQ group (p <0.05). Chemotherapeutically administered ADR appears to cause nephrotoxicity. CLQ administered was found to reduce this toxicity. As a result, we showed that the damage caused by ADR-induced nephrotoxicity decreased with the application of CLQ through the TNF-? and NF-?B p65 inflammation pathway.