Effects of Cisplatin on the Renin-Angiotensin-Aldosterone System and the Regulatory Role of Dexketoprofen Trometamol: An Experimental Study in Rats

INTRODUCTION: Cisplatin is a widely used chemotherapeutic agent whose clinical application is limited by nephrotoxicity. Alterations in the renin–angiotensin–aldosterone system (RAAS) have been implicated in cisplatin-induced renal injury. Dexketoprofen trometamol, a non-selective cyclooxygenase inhibitor commonly prescribed for cancer-related pain, may influence RAAS activity; however, its effects on cisplatin-associated RAAS alterations have not been fully elucidated. This study aimed to evaluate changes in RAAS components following cisplatin administration and to investigate the potential modulatory effect of dexketoprofen trometamol in an experimental rat model.
METHODS: Thirty-two male Wistar albino rats were divided into four groups (n=8): control, cisplatin, cisplatin+dexketoprofen trometamol, and dexketoprofen trometamol alone. Serum levels of renin, aldosterone, angiotensin I, angiotensin II, angiotensin-converting enzyme, and angiotensin II type 1 receptor were measured using ELISA.
RESULTS: Cisplatin administration was associated with significant increases in all evaluated RAAS parameters compared with controls (p < 0.05). Concomitant dexketoprofen trometamol treatment attenuated these alterations and restored RAAS parameters toward control values (p < 0.05). Dexketoprofen trometamol alone did not result in significant changes in RAAS markers.
DISCUSSION AND CONCLUSION: These findings suggest that dexketoprofen trometamol may attenuate cisplatin-induced RAAS activation and potentially contribute to the regulation of nephrotoxic mechanisms

Keywords: Cisplatin, Dexketoprofen trometamol, Renin–angiotensin–aldosterone system