Dexpanthenol reduces fibrosis and aids repair following nerve laceration and neurorrhaphy

Karahan, Gokhan; Kaya, Hüseyin; Eyceyurt, Recep Selçuk; Erdoğan, Mehmet; Yiğittürk, Gürkan; Erbaş, Oytun

doi:10.3892/etm.2021.9639

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…When the literature is examined, it is seen that there is a limited number of studies showing that DXP may have antiinflammatory and neuroprotective effects 6,11,12,24,26,37) . This situation reveals the originality of our study.…”

Section: Discussionmentioning

confidence: 99%

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model

Karatoprak,

Engin,

Sahin

et al. 2024

J Korean Neurosurg Soc

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Objective : Dexpanthenol (DXP), which has known neuroprotective effects, has been shown to be beneficial in various experimental models and ischaemic diseases. The aim of this study was to investigate the possible neuroprotective effects of DXP in a traumatic brain injury (TBI) model. Methods : Thirty-six Wistar-Albino female rats, approximately 6 months old, weighing 220-285 g were used. All rats were subjected to closed head trauma by dropping a weight of 350 g on the parietal region from a height of 50 cm at an angle of 180 degrees in the prepared head trauma model setup. The rats were divided into four groups as control (group 1), trauma (group 2), trauma + DXP (group 3), and DXP (group 4). In group 3, DXP was administered intraperitoneally at a dose of 500 mg/kg for six times at 30 minutes, 6, 12, 24, 36, and 48 hours. In group 4, DXP was administered intraperitoneally simultaneously with group 3 without causing head trauma. Blood samples were taken from all rats 72 hours later for biochemical examination. After blood samples were taken, rats were decapitated under general anaesthesia. Cerebral tissue samples were taken from decapitated rats for immunohistochemical and histopathological examination. Results : Cytokine markers were found to be increased in posttraumatic brain tissue. Malondialdehyde and glutathione reductase levels were lower in group 3 compared to group 2. In addition, superoxide dismutase, glutathione peroxidase and catalase levels were significantly higher in group 3 compared to group 2. In histological evaluation, congestion in the piamater layer, cell infiltration, vascular congestion, hemorrhage and neuronal degeneration were significantly decreased in group 3 compared to group 2. DXP seems to be beneficial in neurological recovery in terms of histological and oxidative changes after head trauma in rats. Conclusion : DXP should be further evaluated for its possible therapeutic effect in TBI.

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Section: Discussionmentioning

confidence: 99%

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model

Karatoprak,

Engin,

Sahin

et al. 2024

J Korean Neurosurg Soc

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“…D-Panthenol is a derivative of vitamin B5 (pantothenic acid) actively metabolized in mammalian tissues by alcohol dehydrogenase and involved in the biosynthesis of coenzyme A [ 19 , 20 ]. PL is considered to exhibit antioxidant properties, especially by the inhibition of lipid peroxidation in vivo [ 21 , 22 , 23 ] and in vitro on isolated mitochondria [ 15 , 16 ]. It is well known that glycerol-associated rhabdomyolysis is accompanied by a release of myoglobin into the bloodstream followed by its oxidation and a release of iron ions, which could activate the Fenton reaction and lipid peroxidation in the kidneys [ 5 , 6 , 7 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of D-Panthenol in Rhabdomyolysis-Induced Acute Kidney Injury

Семенович

Plotnikov

Lukiyenko³

et al. 2022

IJMS

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We investigated the nephroprotective effect of D-panthenol in rhabdomyolysis-induced acute kidney injury (AKI). Adult male Wistar rats were injected with 50% glycerol solution to induce rhabdomyolysis. Animals with rhabdomyolysis were injected with D-panthenol (200 mg/kg) for 7 days. On day 8, we examined AKI markers, renal histology, antioxidant capacity, and protein glutathionylation in kidneys to uncover mechanisms of D-panthenol effects. Rhabdomyolysis kidneys were shown to have pathomorphological alterations (mononuclear infiltration, dilatation of tubules, and hyaline casts in Henle’s loops and collecting ducts). Activities of skeletal muscle damage markers (creatine kinase and lactate dehydrogenase) increased, myoglobinuria was observed, and creatinine, BUN, and pantetheinase activity in serum and urine rose. Signs of oxidative stress in the kidney tissue of rhabdomyolysis rats, increased levels of lipid peroxidation products, and activities of antioxidant enzymes (SOD, catalase, and glutathione peroxidase) were all alleviated by administration of D-panthenol. Its application improved kidney morphology and decreased AKI markers. Mechanisms of D-panthenol’s beneficial effects were associated with an increase in total coenzyme A levels, activity of Krebs cycle enzymes, and attenuation of protein glutathionylation. D-Panthenol protects kidneys from rhabdomyolysis-induced AKI through antioxidant effects, normalization of mitochondrial metabolism, and modulation of glutathione-dependent signaling.

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“…There are studies that mention the positive effects of dexpanthenol on fibrosis. [27,28] The study by Ermis et al [29] showed that dexpanthenol had an effect on preventing bleomycin-induced pulmonary fibrosis. This was attributed to the bleomycin triggering inflammation and collagen deposition with a significant increase in MPO activity, like an increased inflammatory activity, which was prevented by dexpanthenol.…”

Section: Discussionmentioning

confidence: 99%

Comparison of hyperbaric oxygen, ozone, and dexpanthenol therapies in rats with acute lung injury

Yılmaz¹

2022

Eurasian J Pulmonol

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BACKGROUND AND AIM: Acute respiratory distress syndrome (ARDS) is a fatal disease presenting with respiratory failure. Patients with ARDS account for a considerable portion of patients staying in the intensive care unit (ICU). Therefore, advances in the treatment of these patients are of great importance. Direct or indirect injury to the lung initiates an inflammatory process. This results in impaired integrity of the alveolar-capillary membrane, pulmonary edema, and severe hypoxia. The present study compared hyperbaric oxygen (HBO), ozone, and dexpanthenol therapies administered to rats with experimentally induced ARDS, as well as the efficacy of these therapies. METHODS:Thirty-two male Wistar Albino rats were used in the study. The rats were divided into four groups. All groups were administered antibiotherapy for 5 days after administering live Escherichia coli. Group 1 (control group) rats received intraperitoneal saline. Group 2 rats were treated with HBO. Group 3 rats received an oxygen + ozone mixture. Group 4 rats received dexpanthenol. After 5 days, anesthesia was administered to all rats, blood gases were collected from the abdominal aorta, and then the rats were sacrificed. Some of the collected blood was used for cytokine assays. The right lung tissues were used for histopathological examination. The left lung tissues were used to measure enzyme levels. RESULTS:Histopathologically, there were intra-alveolar hemorrhage, edema, intensive inflammatory cell infiltration, fibrosis, collapse, type 2 alveolar cells, and macrophage accumulation in all groups. In terms of fibrosis/alveolar septal thickening, the dexpanthenol group had a significantly lower mean score than the control and HBO groups. In terms of alveolar collapse, the dexpanthenol group had a significantly lower mean score than all other groups. In terms of increased macrophage and type II alveolar cell counts, the ozone group had a significantly lower mean score than all other groups. There was no significant difference in immunohistochemical staining between the groups. In terms of superoxide dismutase levels, the dexpanthenol group had a significantly lower score than the control group. Regarding IL-10 levels, the ozone group had a significantly higher score than the control and HBO groups. The dexpanthenol group had a ORCID:

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Dexpanthenol reduces fibrosis and aids repair following nerve laceration and neurorrhaphy

Cited by 5 publications

References 33 publications

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model

Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model

Protective Effect of D-Panthenol in Rhabdomyolysis-Induced Acute Kidney Injury

Comparison of hyperbaric oxygen, ozone, and dexpanthenol therapies in rats with acute lung injury

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