Papaverine Mitigates Acute Kidney Injury in Feces-Induced Polymicrobial Sepsis Through Regulation of the HMGB1–RAGE Axis
Yazarlar (6)
Doç. Dr. Mehmet Fatih DAŞIRAN Tokat Gaziosmanpaşa Üniversitesi, Türkiye
Doç. Dr. Ahmet Akbaş Karadeniz Teknik Üniversitesi, Türkiye
Bakiye Akbaş Türkiye
Ejder Saylav Bora Türkiye
Dr. Öğr. Üyesi Hatice Aygün Türkiye
Oytun Erbaş Türkiye
| Makale Türü | Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale) | ||
| Dergi Adı | MEDICINA-LITHUANIA (Q1) | ||
| Dergi ISSN | 1010-660X Dergi Bilgileri (2026) | ||
| Dergi Tarandığı Indeksler | SCI-Expanded | ||
| Makale Dili | İngilizce | Basım Tarihi | 03-2026 |
| Cilt / Sayı / Sayfa | 62 / 4 / – | DOI | 10.3390/medicina62040621 |
| Makale Linki | https://doi.org/10.3390/medicina62040621 | ||
| UAK Araştırma Alanları |
Genel Cerrahi
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| Özet |
| Background and Objectives: Sepsis-associated acute kidney injury (SA-AKI) is driven by exaggerated inflammation and oxidative stress, with the HMGB1–RAGE axis playing a pivotal role in amplifying tissue damage. This study aimed to investigate the renoprotective effects of papaverine in a feces-induced peritonitis (FIP) model of sepsis and to explore its impact on HMGB1–RAGE-mediated inflammatory and oxidative pathways. Materials and Methods: Sepsis was induced in male Wistar rats by intraperitoneal injection of fecal slurry (1 g/kg). Animals were treated with papaverine (20 or 40 mg/kg, i.p.) one hour after FIP induction and evaluated at 24 h. Renal function (BUN, creatinine, lactate), inflammatory markers (HMGB1, TNF-α, CRP), oxidative stress (MDA), circulating sRAGE levels, renal NF-κB levels, and histopathological injury scores were assessed. Results: The FIP model resulted in an early mortality rate of 20% and produced marked renal histopathological alterations. Biochemically, FIP increased plasma HMGB1, TNF-α, CRP, MDA, BUN, creatinine, and lactate levels while decreasing sRAGE. Papaverine treatment dose-dependently reduced inflammatory and oxidative markers, restored sRAGE levels, improved renal function parameters, and attenuated histopathological injury. In addition, renal NF-κB levels were significantly elevated in the FIP group compared to controls and were dose-dependently reduced following papaverine treatment. Conclusions: FIP-induced sepsis activates an HMGB1-driven inflammatory–oxidative cascade contributing to SA-AKI. Papaverine confers dose-dependent renoprotection by suppressing HMGB1 … |
| Anahtar Kelimeler |
| papaverine | kidney | sepsis | HMGB1-RAGE | feces-induced peritonitis |
BM Sürdürülebilir Kalkınma Amaçları
| Atıf Sayıları | |
| Web of Science | 1 |
| Google Scholar | 1 |
| PubMed | 1 |