Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring aquaporin-2 levels via regulation of the silent information regulator 1 signaling pathway
Korean Journal of Anesthesiology, cilt.76, sa.5, ss.501-509, 2023 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 76 Sayı: 5
- Basım Tarihi: 2023
- Doi Numarası: 10.4097/kja.23207
- Dergi Adı: Korean Journal of Anesthesiology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, MEDLINE, Directory of Open Access Journals
- Sayfa Sayıları: ss.501-509
- Anahtar Kelimeler: Apoptosis, Caspase 3, Dexpanthenol, Kidney, Oxidative stress, Sirtuin 1
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
Background: Acute kidney injury (AKI) is a serious pathology that causes dysfunction in concentrating urine due to kidney damage, resulting in blood pressure dysregulation and increased levels of toxic metabolites. Dexpanthenol (DEX), a pantothenic acid analog, ex-hibits anti-inflammatory and anti-apoptotic properties in various tissues. This study inves-tigated the protective effects of DEX against systemic inflammation-induced AKI. Methods: Thirty-two female rats were randomly assigned to the control, lipopolysaccha-ride (LPS), LPS+DEX, and DEX groups. LPS (5 mg/kg, single dose on the third day, 6 h before sacrifice) and DEX (500 mg/kg/day for 3 days) were administered intraperitoneally. After sacrifice, blood samples and kidney tissues were collected. Hematoxylin and eosin, caspase-3 (Cas-3), and tumor necrosis factor alpha (TNF-α) staining were performed on the kidney tissues. The total oxidant status (TOS) and total antioxidant status were mea-sured using spectrophotometric methods. Aquaporin-2 (AQP-2), silent information regulator 1 (SIRT1), and interleukin-6 (IL-6) were detected using quantitative reverse transcription-polymerase chain reaction analysis. Results: Histopathological analysis revealed that DEX treatment ameliorated histopathological changes. In the LPS group, an increase in the blood urea nitrogen, creatinine, urea, IL-6, Cas-3, TNF-α, and TOS levels and oxidative stress index was observed compared with the control group, whereas AQP-2 and SIRT1 levels decreased. DEX treatment re-versed these effects. Conclusions: DEX was found to effectively prevent inflammation, oxidative stress, and apoptosis in the kidneys via the SIRT1 signaling pathway. These protective properties sug-gest DEX’s potential as a therapeutic agent for the treatment of kidney pathologies.