Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring AQP-2 levels via regulating SIRT-1 signaling pathway

Acute kidney injury (AKI) is a serious pathology, causing dysfunction of urination and concentration due to damage to kidneys, resulting with blood pressure dysregulation and increased toxic metabolites. Dexpanthenol (DEX), a pantothenic acid analog, has anti-inflammatory and anti-apoptotic properties in various tissues. This study aimed to investigate the protective effects of DEX in systemic inflammation induced AKI. Thirty-two female rats were randomly assigned as control, lipopolysaccharide (LPS), LPS+DEX and DEX groups. LPS (5 mg/kg, single dose on 3rd day, 6 hours before sacrification) and DEX (500 mg/kg/d for 3 days) were administered intraperitoneally. After sacrification, blood samples and kidney tissues were collected. Hematoxylin-eosin, caspase-3 (Cas-3) and tumor necrosis factor alpha (TNF-α) staining were performed on kidney tissues. Total oxidant status (TOS) and total antioxidant status levels were measured with spectrophotometric method. Aquaporin-2 (AQP-2), silent information regulator gene-1 (SIRT1) and interleukin-6 (IL-6) gene expressions were detected with qRT-PCR. In the histopathological analysis, it was observed that DEX ameliorated histopathological changes. In the LPS group, there was an increase in blood urea nitrogen, creatinine, urea, TOS, oxidative stress index, IL-6, Cas-3, and TNF-α levels compared to the control group, while AQP-2 and SIRT1 levels were decreased. However, treatment with DEX reversed all these changes. In conclusion, DEX was found to be effective in preventing inflammation, oxidative stress, and apoptosis in the kidney through the SIRT1 signaling pathway. Thus, the protective properties of DEX suggest that it may be a potential therapeutic agent for kidney pathologies.