Effects of Cisplatin on the Renin-Angiotensin-Aldosterone System and the Regulatory Role of Dexketoprofen Trometamol: An Experimental Study in Rats
Eastern Journal of Medicine, cilt.31, sa.3, ss.419-426, 2026 (Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 31 Sayı: 3
- Basım Tarihi: 2026
- Doi Numarası: 10.5505/ejm.2026.48285
- Dergi Adı: Eastern Journal of Medicine
- Derginin Tarandığı İndeksler: Scopus, EMBASE, TR DİZİN (ULAKBİM), Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Sayfa Sayıları: ss.419-426
- Anahtar Kelimeler: Cisplatin, Dexketoprofen trometamol, Nephrotoxicity, Rat model, Renin–angiotensin–aldosterone system
- Van Yüzüncü Yıl Üniversitesi Adresli: Evet
Özet
Cisplatin is a platinum-based chemotherapeutic agent used in the treatment of various malignancies; however, its clinical use is limited by nephrotoxic effects. Evidence sugge sts that disturbances in the renin–angiotensin–aldosterone system (RAAS) contribute to cisplatin-induced renal injury. Therefore, 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. Thirty-two male Wistar albino rats were randomly allocated into four groups (n=8): control, cisplatin (CIS), cisplatin plus dexketoprofen trometamol (CIS+DKT), and dexketoprofen trometamol (DKT). Cisplatin was administered intraperitoneally to induce nephrotoxicity, whereas dexketoprofen trometamol was given according to the experimental protocol. Serum levels of aldosterone (ALD), renin, angiotensin I (Ang I), angiotensin II (Ang II), angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor (AT1R) were determined using ELISA kits. Cisplatin administration markedly increased serum ALD, renin, Ang I, Ang II, ACE, and AT1R levels compared with the control group (p<0.05), indicating activation of the RAAS pathway. In contrast, combined treatment with dexketoprofen trometamol significantly reduced these parameters relative to the CIS group (p<0.05). No significant differences were observed between the DKT and control groups. The results of the present study suggest that cisplatin-induced nephrotoxicity is associated with disturbances in the renin– angiotensin–aldosterone system. Dexketoprofen trometamol may attenuate these alterations and contribute to the restoration of RAAS homeostasis. These findings indicate that dexketoprofen trometamol may have a potential modulatory role in cisplati n-related renal injury.