Protective effect of dexpanthenol against nephrotoxic effect of amikacin: An experimental study

Doğan, Elif; Erkoç, Reha; Ekinci, İskender; Hamdard, Jamshid; Döner, Barış; Çıkrıkçıoğlu, Mehmet Ali; Karatoprak, Cumali; Çoban, Ganime; Özer, Ömer Faruk; Kazancıoğlu, Rümeyza

doi:10.1016/j.biopha.2017.03.019

Cited by 14 publications

(6 citation statements)

References 20 publications

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“…Microvascular damage can lead to the impairment of tubular function and tissue oxygenation, resulting in the generation of ROS that exacerbates inflammation and tissue damage [ 31 ]. The decrease in the OSI following DEX treatment in our study is thus consistent with previous study, which have reported that DEX decreases OSI in a model of amikacin-induced nephrotoxicity [ 18 ]. The imbalance in oxidative stress is dependent on an insufficient response of the SIRT1 signaling pathway, which plays a crucial role in regulating inflammation and apoptosis.…”

Section: Discussionsupporting

confidence: 93%

Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring aquaporin-2 levels via regulation of the silent information regulator 1 signaling pathway

Özden¹,

Aşçı²,

Büyükbayram³

et al. 2023

Korean J Anesthesiol

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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, exhibits anti-inflammatory and anti-apoptotic properties in various tissues. This study investigated the protective effects of DEX against systemic inflammation-induced AKI. Methods: Thirty-two female rats were randomly assigned to the control, lipopolysaccharide (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/d for 3 d) 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 measured 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 reversed 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 suggest DEX’s potential as a therapeutic agent for the treatment of kidney pathologies.

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Section: Discussionsupporting

confidence: 93%

Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring aquaporin-2 levels via regulation of the silent information regulator 1 signaling pathway

Özden¹,

Aşçı²,

Büyükbayram³

et al. 2023

Korean J Anesthesiol

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“…It has been shown that disturbances in the metabolism of PA, taurine and phenylalanine in the kidney cortex are associated with the development of acute kidney injury in sepsis [ 32 ]. In vivo studies demonstrated that DXP reduced the nephrotoxicity of amikacin and the hepatotoxicity of cisplatin [ 9 , 33 ]. These findings encouraged us to further investigate the effects of DXP on kidney and liver injury in mice model of sepsis.…”

Section: Discussionmentioning

confidence: 99%

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

2022

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Sepsis is capable of causing systemic infections resulting in multiple organ damage. Dexpanthenol (DXP) has been reported to protect against kidney and liver injury. Therefore, this paper attempts to explore the role of DXP in sepsis-induced kidney and liver injury. A mice model of sepsis was established using the cecal ligation and puncture (CLP) method. The expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and monocyte chemoattractant protein (MCP)-1 in the serum of mice were measured utilizing enzyme linked immunosorbent assay (ELISA). Additionally, the damage of kidney and liver tissues in CLP-induced mice was determined by their respective commercial kits, western blot, and hematoxylin–eosin (HE) staining kits. The apoptosis of kidney and liver tissues in CLP-induced mice was assessed by means of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot. It was observed that DXP decreased the expressions of TNF-α, IL-1β, IL-6, and MCP-1 in the serum of CLP-induced mice, attenuated the functional impairment, pathological damage, inflammation, and cell apoptosis of kidney tissue. Meanwhile, DXP decreased the functional impairment of liver in CLP-induced mice, reduced the levels of inflammatory factors and antioxidant enzymes, attenuated liver pathological damage, and decreased cell apoptosis in liver tissues. In conclusion, DXP attenuates inflammatory damage and apoptosis in kidney and liver organs in a sepsis model.

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“…The first limiting factor was that we did not studied serum and tissue parameters indicative of nephrotoxicity although the latter is the main most serious side effect of Cis ( 28 ). In the present study we had the opportunity to show both the nephrotoxic effects of Cis and the nephroprotective effects of Dexp ( 29 ). However, as the study designs solely focused on the liver, renal effects were unfortunately ignored.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of dexpanthenol against cisplatin‑induced hepatotoxicity

et al. 2018

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The aim of the present study was to investigate the protective effect of dexpanthenol (Dexp) against cisplatin (Cis)-induced hepatotoxicity. Thirty-two Sprague Dawley rats were divided into four groups: Control group (n=8), Dexp group (n=8, 500 mg/kg/ip/daily single dose/3 days Dexp), Cis group (n=8, 7 mg/kg/ip/single dose Cis) and Cis+Dexp group (n=8, 500 mg/kg/ip/daily single dose/3 days Dexp +7 mg/kg/ip/single dose Cis). MDA, CAT, GSH, GSH-Px, TOS, TAS, OSI, Total Nitrit, IL-1β, IL-6 and TNF-α levels were analyzed in liver tissue samples. After paraffinization of liver tissue samples, histopathological (congestion, loss of glycogen, number of Kupffer cells) and immunohistochemical (caspase-3 expression) parameters were assessed on the paraffinized liver sections. GSH, TAS, TOS, OSI, Tot Nit, L-Arginine, ADMA and SDMA levels were measured in the serum samples. Statistically significant differences were found between the groups in terms of all liver tissue biochemical parameters, with the exception of IL-1β and TNF-α levels. GSH, CAT, GSH-Px, TAS and Tot Nit levels were significantly higher in the Cis+Dexp group compared to the Cis group, whereas MDA, TOS, OSI and IL-6 levels were higher in the Cis group. Similarly, serum GSH, TAS, Tot Nit levels were higher in the Cis+Dexp group whereas TOS, L-Arginine, ADMA and SDMA levels were higher in Cis group. There were statistically significant differences between Control and Cis groups in terms of congestion increase, increase of glycogen loss, increase of Kupffer cell number and increase of caspase-3 expression (P<0.001). There was a statistically significant difference between the Cis and the Cis+Dexp groups in terms of histopathologic parameters, with the exception of congestion (P<0.001). To conclude, histopathological, immunohistochemical, and biochemical results of this study demonstrated that Dexp has a protective effect against Cis-induced hepatotoxicity.

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Protective effect of dexpanthenol against nephrotoxic effect of amikacin: An experimental study

Cited by 14 publications

References 20 publications

Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring aquaporin-2 levels via regulation of the silent information regulator 1 signaling pathway

Dexpanthenol protects against lipopolysaccharide-induced acute kidney injury by restoring aquaporin-2 levels via regulation of the silent information regulator 1 signaling pathway

Dexpanthenol attenuates inflammatory damage and apoptosis in kidney and liver tissues of septic mice

Protective effect of dexpanthenol against cisplatin‑induced hepatotoxicity

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