Effects of carnosic acid on renal injury-related parameters and iNOS immunoreactivity in an experimental model of contrast-associated acute kidney injury
Renal Failure, cilt.48, sa.1, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 48 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1080/0886022x.2026.2719144
- Dergi Adı: Renal Failure
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Directory of Open Access Journals, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: carnosic acid, Contrast-associated acute kidney injury, inducible nitric oxide synthase, oxidative stress, renal tubular injury
- Trakya Üniversitesi Adresli: Evet
Özet
Contrast-associated acute kidney injury (CA-AKI) remains a clinically relevant complication of iodinated contrast exposure. Carnosic acid possesses antioxidant and anti-inflammatory properties, but its effects on renal biochemical injury, tubular damage, and inducible nitric oxide synthase (iNOS) immunoreactivity in CA-AKI remain unclear. This study evaluated carnosic acid in an experimental rat model of CA-AKI. Twenty-four adult male rats were randomly assigned to control, CA-AKI, or CA-AKI plus carnosic acid groups (n = 8 each). CA-AKI was induced by 24-h restriction, furosemide, and intravenous iohexol. After contrast exposure, carnosic acid was administered therapeutically at 30 mg/kg once daily for 5 days through an orogastric catheter. Serum urea, creatinine, sodium, potassium, and creatine kinase levels were measured. Tubular injury was scored semi-quantitatively, and iNOS immunoreactivity was assessed using the H-score. Groups were compared using the Kruskal–Wallis test with Dunn–Bonferroni post hoc analysis. Compared with controls, the CA-AKI group had significantly higher urea, creatinine, potassium, creatine kinase, tubular injury scores, and iNOS H-scores and lower sodium levels. Compared with untreated CA-AKI, carnosic acid treatment significantly reduced urea and creatine kinase levels and increased sodium levels. Creatinine concentrations, tubular injury scores, and iNOS H-scores were numerically lower after treatment, but pairwise differences were not statistically significant. Thus, carnosic acid improved selected biochemical parameters, while its apparent histopathological and iNOS-related effects remained inconclusive. These findings support a possible but limited protective effect in this experimental setting. Further studies incorporating molecular validation and dose and timing protocols are required to clarify its renoprotective potential and mechanisms.