Dexpanthenol Research Articles

Effect of Dentifrice Ingredients on Volume and Vitality of a Simulated Periodontal Multispecies Biofilm.

The aim of this in vitro study was to investigate the effect of different toothpaste ingredients on biofilm volume and vitality in an established non-contact biofilm removal model. A multi-species biofilm comprising Porphyromonas gingivalis, Streptococcus sanguinis, and Fusobacterium nucleatum was grown on protein-coated titanium disks. Six disks per group were exposed to 4 seconds non-contact brushing using a sonic toothbrush. Four groups assessed slurries containing different ingredients, i.e., dexpanthenol (DP), peppermint oil (PO), cocamidopropyl betaine (CB), and sodium hydroxide (NaOH), one positive control group with the slurry of a toothpaste (POS), and a negative control group with physiological saline (NEG). Biofilm volume and vitality were measured using live-dead staining and confocal laser scanning microscopy. Statistical analysis comprised descriptive statistics and inter-group differences. In the test groups, lowest vitality and volume were found for CB (50.2 ± 11.9%) and PO (3.6 × 105 ± 1.8 × 105 µm3), respectively. Significant differences regarding biofilm vitality were found comparing CB and PO (p = 0.033), CB and NEG (p = 0.014), NaOH and NEG (p = 0.033), and POS and NEG (p = 0.037). However, no significant inter-group differences for biofilm volume were observed. These findings suggest that CB as a toothpaste ingredient had a considerable impact on biofilm vitality even in a non-contact brushing setting, while no considerable impact on biofilm volume was found.

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

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. 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. 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. DXP should be further evaluated for its possible therapeutic effect in TBI.

Dexpanthenol exhibits antiapoptotic and anti-inflammatory effects against nicotine-induced liver damage by modulating Bax/Bcl-xL, Caspase-3/9, and Akt/NF-κB pathways.

Chronic tobacco use can lead to liver damage and inflammation due to the accumulation of various toxins in the body. This study aimed to investigate the correlation between the molecular mechanisms of nicotine-induced liver injury, the caspase cascade, and the Akt/NF-κB signaling pathway, as well as the protective effects of dexpanthenol (DEX). Male rats were subjected to intraperitoneal injections of nicotine at a concentration of 0.5 mg/kg/day and/or DEX at a concentration of 500 mg/kg/day for 8 weeks. After the treatment period, liver function tests were conducted on serum samples, and tissue samples were analyzed for protein levels of Akt, NF-κB, Bax, Bcl-xL, Caspase-3, and Caspase-9, along with histopathological changes. Additionally, assessments of oxidative stress markers and proinflammatory cytokines were carried out. Nicotine administration led to elevated levels of IL-6, IL-1β, MDA, TOS, and oxidative stress index, accompanied by decreased TAS levels. Moreover, nicotine exposure reduced the p-Akt/Akt ratio, increased NF-κB, Bax, Caspase-3, and Caspase-9 protein levels, and decreased the antiapoptotic protein Bcl-xL levels. DEX treatment significantly mitigated these effects, restoring the parameters to levels comparable to those of the control group. Nicotine-induced liver injury resulted in oxidative stress, inflammation, and apoptosis, mediated by Bax/Bcl-xL, Caspase-3, Caspase-9, and Akt/NF-κB pathways. Conversely, DEX effectively attenuated nicotine-induced liver injury by modulating apoptosis through NF-κB, Caspase-3, Caspase-9, Bax inhibition, and Bcl-xL activation.

Comparison of the effects of alpha lipoic acid and dexpanthenol in an experimental tracheal reconstruction animal model.

To investigate the positive effects of intraperitoneal administration of alpha-lipolic acid (ALA) and dexpanthenol (DXP) on wound healing after tracheal surgery in rats. The study was carried out at Necmettin Erbakan University, Konya, Turkey, from January 2014-2019. A total of 30 healthy and adult Sprague-Dawley type female rats were included in the study. For the experiment, rats were randomly divided into 3 groups: ALA group (n=10), DXP group (n=10), and control group (n=10). After trachea surgery, 100mg/kg/day ALA was given to group ALA and 100mg/kg/day intraperitoneal DXP to group DXP for 15 days, and the rats were sacrificed on the 21st day. The excised tracheal sections were evaluated and graded for inflammatory cell infiltration, angiogenesis, fibroblast proliferation, collagen deposition, and epithelial regeneration to evaluate wound healing. Inflammation was found to be less in both the ALA and DXP groups. With the Mann-Whitney test, it was determined that inflammation was less in the ALA group than in the DXP group (C-D [p=0.097] and C-A [p=0.024]). On the other hand, no statistically significant difference was found in epithelial regeneration (p=0.574; >0.05), angiogenesis (p=0.174; >0.05), fibroblast proliferation, and collagen deposition (p=0.102; >0.05). Alpha-lipolic acid injected intravenously after tracheal reconstruction in patients can prevent restenosis by reducing inflammation without adversely affecting wound healing.

Dexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathway.

Dexpanthenol (DEX), a subtype of vitamin B5, plays an important role in anabolic reactions, cellular energy and regeneration in the body. Nicotine has been shown to induce kidney damage through the mechanisms of oxidative stress and apoptosis. The purpose of this study was to investigate the potential protective effects of DEX against nicotine-induced kidney damage through modulation of the AKT/Nrf2/HO-1 signaling pathway.Male rats were intraperitoneally administered with 0.5mg/kg/day nicotine and/or 500mg/kg/day DEX for 8weeks. Following administration, renal function tests were conducted on serum samples, and histopathological examinations and analysis of oxidative stress markers and antioxidant enzymes were performed on tissue samples. Protein levels of Akt, Nrf-2, HO-1, Bcl-xL, and Caspase-9 were also evaluated.Nicotine administration resulted in decreased protein levels of p-Akt, Nrf-2, HO-1, and Bcl-xL and increased Caspase-9 protein levels. In addition, nicotine administration caused an increase in MDA, TOS, and OSI levels and a decrease in GSH, GSH-Px, GST, CAT, SOD, and TAS levels. Additionally, BUN and Creatinine levels increased after nicotine administration. DEX administration positively regulated these parameters and brought them closer to control levels.Nicotine-induced kidney injury caused apoptosis and oxidative stress through Caspase-9 activation. DEX effectively prevented nicotine-induced kidney damage by increasing intracellular antioxidant levels and regulating apoptosis through Bcl-xL activation. These findings suggest that DEX has potential as a protective agent against nicotine-induced kidney damage.

Study of factors affecting the in vitro release of dexpanthenol from solutions and topical semi-solid preparations

The aim. To identify the factors influencing the in vitro release of dexpanthenol (DP) from solutions and semi-solid preparations.
 Materials and methods. Dispersed systems containing 5.0 % DP were studied: solutions that were Newtonian liquids and semi-solid preparations (creams, gels and ointment) with non-Newtonian flow behaviour. Rheological studies were performed by rotational viscometry. In vitro release tests were performed using vertical diffusion cells. The content of DP in the receptor medium was determined by liquid chromatography.
 Results. It has been shown that the greatest values of release parameters of DP were characteristic of its aqueous solution; they decreased when propylene glycol (PG), macrogol 400 (M400), and poloxamer 338 (P338) were added but remained at a high enough level. The inclusion of cationic surfactant and cetostearyl alcohol (CSA) (0.5 : 4.5 % m/m) into the Newtonian liquid led to the formation of disperse system with a plastic flow behaviour and to significant decrease in the DP release. In the case of a cream containing a non-ionic surfactant and CSA, the release parameters of DP were also at a low level. The release of DP from the w/o emulsion-based ointment was minimal. Compared to DP aqueous solution, the rate of DP release from a carbomer-based gel decreased by 2.8 times; when 20 % of a mixture of PG and M400 (10 : 10 % m/m) was added to such a gel, the rate of drug release decreased by another 1.5 times. The fastest and most complete release of DP was observed in the case of the P338-based disperse system, which transformed from a Newtonian liquid into a gel at 32 °C.
 Conclusions. In vitro release of DP depended on the type of base; rapid and complete release of DP was characteristic of its aqueous solution, and minimal release was observed in the case of hydrophobic ointment. The use of CSA in combination with a surfactant or carbomer to create bases for semi-solid preparations with plastic flow behaviour was a considerable factor that significantly slowed down the release of DP from them. The greatest values of the release parameters of DP were observed in the case of a gel based on P338

Efficacy of inclusion of vitamin U and provitamin B5 combination in the complex therapy of primary osteoarthritis against the background of gastrogenic exocrine pancreatic insufficiency

Clinical comorbidities at osteoarthritis (OA) complicate its treatment. The number and nature of various comorbid conditions determine the severity of the condition in patients with multimorbidity. However, apart from the common risk factors such as aging and obesity, little is known about the biological plausibility of explaining the co‑occurrence of OA and comorbidities. According to the European Alliance of Associations for Rheumatology, EULAR, and the National Institute of Health and Nursing, the diagnosis and treatment of specific comorbidities, as well as understanding their nature in OA, are important for choosing the best treatment tactics.
 Objective — to investigate efficacy of inclusion of vitamin U and provitamin B5 combination in the complex therapy of patients with primary OA in comorbidity with gastrogenic exocrine pancreatic insufficiency (EPI) for the correction of clinical syndromes.
 Materials and methods. Examinations involved 61 patients with primary OA in comorbidity with gastrointestinal diseases, accompanied by EPI of gastrogenic genesis without exacerbation. The comparison group consisted of 30 practically healthy people. All patients were divided into two comparable groups: group 1 (n=30) received a course of basic therapy drugs, namely: nonsteroidal anti‑inflammatory drugs, chondroprotectors and/or chondrostimulators, antispasmodics, prokinetics, proton pump inhibitors, enzyme agents (pancreatin); group 2 (n=31), in addition to the course of basic therapy, received a course of the vitamin drug combination of vitamin U and provitamin B5, 2 tablets once a day for 6 weeks. The calculation of the WOMAC index (Western Ontario and McMaster University) was used to assess the articular status of patients with primary OA, as well as the effectiveness of the treatment measures. Gastrointestinal Symptom Rating Scale (GSRS) questionnaire was used to assess gastrointestinal symptoms.
 Results. The proposed complex treatment of patients with primary OA with gastrogenic EPI with the additional inclusion of a vitamin preparation combination of vitamin U and provitamin B5 contributed to more significant regression of WOMAC indices compared to that during protocol treatment (the total WOMAC index decreased by 16.03% against 9.10%, respectively) and indicators of the scales of the GSRS questionnaire in comparison with the subgroup that received treatment according to the protocol (in total — by 35.96% vs. 22.19%, p <0.05),
 Conclusions. The study results showed the advisability of using a vitamin medication, a combination of vitamin U and provitamin B5. in the treatment of patients with primary OA with gastrogenic EPI.

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.

Dexpanthenol ameliorates doxorubicin-induced lung injury by regulating endoplasmic reticulum stress and apoptosis.

Doxorubicin (DOX), which is used as a chemotherapeutic agent in the treatment of tumors, has limited use due to its toxicity in various organs and tissues. One of the organs where DOX has a toxic effect is the lung. DOX shows this effect by increasing oxidative stress, inflammation, and apoptosis. Dexpanthenol (DEX), a homologue of pantothenic acid, has anti-inflammatory, antioxidant, and anti-apoptotic properties. Therefore, the purpose of our investigation was to explore how DEX could counteract the harmful effects of DOX on the lungs. Thirty-two rats were used in the study, and 4 groups were formed (control, DOX, DOX + DEX, and DEX). In these groups, parameters of inflammation, ER stress, apoptosis, and oxidative stress were evaluated by immunohistochemistry, RT-qPCR, and spectrophotometric methods. In addition, lung tissue was evaluated histopathologically in the groups. While CHOP/GADD153, caspase-12, caspase-9, and Bax gene expressions increased in the DOX group, Bcl-2 gene expression levels significantly decreased. In addition, changes in Bax and Bcl-2 were supported immunohistochemically. There was a significant increase in oxidative stress parameters and a significant decrease in antioxidant levels. In addition, an increase in inflammatory marker (TNF-α and IL-10) levels was determined. There was a decrease in CHOP/GADD153, caspase-12, caspase-9, and Bax gene expressions and an increase in Bcl-2 gene expression in the DEX-treated group. In addition, it was determined that there was a decrease in oxidative stress levels and inflammatory findings. The curative effect of DEX was supported by histopathological findings. As a result, it was experimentally determined that DEX has a healing effect on oxidative stress, ER stress, inflammation, and apoptosis in lung damage caused by DOX toxicity.

Dexpanthenol prevents ovarian ischemic damage via antioxidant mechanisms in rats

Ovarian torsion is a gynecological emergency characterized by ovarian ischemic damage. This study aimed to investigate the possible protective effects of dexpanthenol (DEX)-an antioxidant molecule-against ovarian ischemic damage in rats. The rats were simple randomly grouped into (1) Sham group (n=8); (2) Ischemia (I) group (n=8) (2 hours of I in ovaries); (3) DEX+I group (n=8) (500 mg/kg DEX administration 30 minutes before 2 hours of I.) The removed ovaries were examined histopathologically and biochemically. In the DEX+I group, necrosis-pycnosis severity was significantly reduced compared to the I group; but congestion-hemorrhage severity was similar. In the I group, malondialdehyde (MDA) and total oxidant status (TOS) levels were slightly increased, and glutathione (GSH) levels were significantly decreased compared to the Sham group. In the DEX+I group, MDA and TOS levels were slightly reduced and GSH levels were slightly increased compared to the I group. DEX prevents ischemic damage in rat ovaries via an antioxidant effect. Further research is needed to support our findings.

Neuroprotective Effects of Dexpanthenol on Rabbit Spinal Cord Ischemia/Reperfusion Injury Model

Dexpanthenol (DXP) reportedly protects tissues against oxidative damage in various inflammation models. This study aimed to evaluate its effects on oxidative stress, inflammation, apoptosis, and neurological recovery in an experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. Rabbits were randomized into 5 groups of 8 animals each: group 1 (control), group 2 (ischemia), group 3 (vehicle), group 4 (methylprednisolone, 30mg/kg), and group 5 (DXP, 500mg/kg). The control group underwent laparotomy only, whereas other groups were subjected to spinal cord ischemia by aortic occlusion (just caudal to the 2 renal arteries) for 20min. After 24h, a modified Tarlov scale was employed to record neurological examination results. Malondialdehyde and caspase-3 levels and catalase and myeloperoxidase activities were analyzed in tissue and serum samples. Xanthine oxidase activity was measured in the serum. Histopathological and ultrastructural evaluations were also performed in the spinal cord. After SCIRI, serum and tissue malondialdehyde and caspase-3 levels and myeloperoxidase and serum xanthine oxidase activities were increased (P<0.05-0.001). However, serum and tissue catalase activity decreased significantly (P<0.001). DXP treatment was associated with lower malondialdehyde and caspase-3 levels and reduced myeloperoxidase and xanthine oxidase activities but increased catalase activity (P<0.05-0.001). Furthermore, DXP was associated with better histopathological, ultrastructural, and neurological outcome scores. This study was the first to evaluate antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects of DXP on SCIRI. Further experimental and clinical investigations are warranted to confirm that DXP can be administered to treat SCIRI.

Lip mesotherapy with dexpanthenol in the treatment of isotretinoin-induced cheilitis.

Cheilitis is the most common mucocutaneous side effect of isotretinoin (ISO). Dexpanthenol (DXP) increases fibroblast proliferation and re-epithelialization in wound healing. We aimed to investigate the effect of DXP-mesotherapy in ISO-induced cheilitis in this study. This study was conducted on patients who had been using ISO (0.5-1mg/kg/day) for at least 2months. Twenty-five patients who administered DXP-mesotherapy (mesotherapy group) and 33 patients without the procedure (control group, only ointment) participated in this study. All patients were prescribed only hamamelis virginiana distillate in ointment form as a lip balm. The efficacy of the treatment was interpreted by the change in lip balm use frequency, quality of life, and Isotretinoin Cheilitis Grading Scale (ICGS). There was a statistically significant decrease in all ICGS-subgroups scores in the mesotherapy group after 1month compared with the baseline (p=<0.001), although in the controls, erythema, crust, and fissure scores significantly increased (p=0.001, p=0.002).While there was no difference between the groups in terms of ICGS total scores at baseline, there was a significant difference after 1month in favor of the mesotherapy group (p<0.001). In the mesotherapy group, lip balms were needed significantly less frequently and there was a significant improvement in quality of life compared with both the control group and at baseline after 1month (both; p<0.001). On the other hand, the control patients suffered more from cheilitis and dryness than at baseline (p<0.001). Dexpanthenol-mesotherapy seems to be a safe, and so effective method in management of ISO-related cheilitis.

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

ABSTRACT 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.

Health Effects of Dyes, Minerals, and Vitamins Used in Cosmetics

The average woman uses 12 different cosmetic products every day, but they can have a negative effect on human health. Therefore, in recent years, consumer preferences have changed towards buying natural or ecological cosmetics free from preservatives or unnecessary dyes. The aim of this work is to discuss the use of dyes, minerals, and vitamins in cosmetics in terms of their safety and impact on human health. These substances are very important in the cosmetics industry. Most of them are of natural origin. Some minerals used in the production of face masks or creams are recommended to work against inflammations such as ulcers and acne. Clay minerals have exceptional qualities, among others, low or no toxicity and high bio-compatibility. However, some of them may be harmful. For example, the safety of using talc has been widely debated in recent years. Cosmetic-grade talc cannot contain detectable fibrous asbestos minerals. Moreover, talc should not be applied to the skin when the epidermal barrier is missing or significantly disrupted. The use of talc in cosmetic products in the European Union is restricted. Vitamins are one of the most commonly used, biologically active, and easily accessible components in cosmetics. For example, provitamin B5 (D-panthenol) is a bioactive substance. In cosmetic preparations, it has a softening, repairing, and anti-inflammatory effect and is responsible for regulating sebum secretion. However, some vitamins may be harmful to human health. For example, the use of skin-whitening cosmetics containing vitamin C causes allergic contact dermatitis, whereas the most common adverse effect of topical use of vitamin A is skin irritation, erythema, and peeling. Dyes, which are used to color cosmetics, do not improve the condition of the skin, hair, or nails. Some of them may be harmful to human health. For example, the dye CI 60730 (Acid Violet 43) is prohibited for use in eye products and cosmetics that have contact with mucous membranes. In conclusion, some of the popular cosmetic ingredients discussed in this paper may exert a negative influence on human health, and many of these harmful effects have been discovered recently. Therefore, there is a need for further studies on the possible negative effects of dyes, minerals, and vitamins used in cosmetic products.

Protective effect of dexpanthenol on cisplatin induced nephrotoxicity in rats

ABSTRACT Cisplatin (CIS) is an antineoplastic agent used for treating solid organ tumors. Toxic side effects of CIS treatment include nephrotoxicity, neurotoxicity, ototoxicity, myelosuppression and hepatotoxicity. Dexpanthenol (DEX) exhibits antioxidant and anti-inflammatory effects and protective effects against free oxygen radicals. We investigated the protective effects of DEX on CIS induced nephrotoxicity. Animals were divided into four groups of 10. The control group was given saline. The DEX group was treated with DEX for 10 days. The CIS group was treated with a single dose of CIS. The DEX + CIS group was given a single dose of CIS followed by DEX for 10 days. We found increased levels of malondialdehyde (MDA), blood urea nitrogen (BUN) and creatinine, while superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and myeloperoxidase (MPO) levels were decreased in the CIS group. MDA, BUN and creatinine levels were decreased, while SOD, CAT, GPx and MPO levels were increased in the DEX + CIS group. Renal tubule damage, inflammation and histopathology scores were significantly higher in the CIS group than the control. The DEX + CIS group exhibited less renal tubule damage and inflammation, and lower histopathological assessment scores than the CIS group. Significant cortical tubule damage and interstitial inflammation were observed in the CIS group. Tubule damage was slightly less, and mild tubule dilation and less cast formation were observed in the DEX + CIS group; also, inflammation was less severe than for the CIS group. DEX may have therapeutic potential for treating CIS induced nephrotoxicity due to its antioxidant and anti-inflammatory properties.

Dexpanthenol and ascorbic acid ameliorate colistin-induced nephrotoxicity in rats.

Colistin is a potent antibiotic which is mainly preferred in the treatment of multidrug-resistant (MDR) gram-negative bacilli. However, due to the increased risk of acute kidney injury following its use, the clinical application is limited. This nephrotoxicity is known to be induced by oxidative stress and related inflammation. In this study on rats, potent antioxidants Dexpanthenol (DEX) and Ascorbic acid (Vit C) have been administered in combination with Colistin to find out whether they would weaken Colistin's nephrotoxic effects. Inflammation biomarkers were studied with enzyme-linked immunosorbent assay (ELISA) kits, and oxidative stress biomarkers were studied with different photometric methods in blood and tissue samples taken after treatment with DEX and Vit C in rats with colistin nephrotoxicity. In addition, inflammation and necrosis in the kidney tissues were examined pathologically. It has been observed in the serum and tissue samples that DEX and Vit C decrease oxidative stress and inflammation biomarkers, therefore acting as nephroprotective agents. These compounds have been found to ameliorate the nephrotoxic effects of Colistin, which were demonstrated in the rats treated with Colistin, as well as the combinations.

Modulating Oxidative Stress Indices and Thiol-Disulfide Balance in the Brain Structures by Pantothenic Acid Derivatives in an Experimental Model of Parkinson’s Disease

Abstract—We studied changes in the indices of free-radical oxidation and thiol-disulfide status in the brain structures in the experimental model of Parkinson’s disease (PD) induced by administration of rotenone to rats. Pantothenic acid derivatives, such as panthenol (PL), pantethine (PT), and homopantothenic acid (HPA) were used as neuromodulators. It was found that redox imbalance in the brain induced by rotenone is accompanied by the activation of free-radical processes, pronounced inhibition of antioxidant defense, a considerable decrease in the glutathione system reduction potential, and increased protein glutathionylation. The strongest changes were in the basal ganglia of the brain. PL and PT but not HPA, decrease the changes in the free-radical oxidation and thiol-disulfide balance in the brain structures. During experimental neurotoxicosis, the mechanisms of neuroprotective action of PL and PT, which are linked with the changes in the biosynthesis of CoA, are, obviously, related to their ability to increase the reduction potential of the glutathione system, thus mitigating the effects of oxidative stress.

POSSIBILITIES OF COMPLEX CORRECTION OF MORPHOLOGICAL GASTRODUODENAL CHANGES WITH COMORBIDITY OF CHRONIC PANCREATITIS AND CHRONIC H. PYLORI – GASTRITIS

The aim: To investigate the efficacy of Doctovit, a combination of dexpanthenol (provitamin B5) and methylmethionine (vitamin U), in the treatment of patients with chronić pancreatitis in combination with chronic erosive gastritis associated with H. pylori by studying the dynamics of stomach lining morphological changes. Materials and methods: Forty-five outpatients with CP and H.pylori CG were examined. The degree of excretory insufficiency of the pancreas was determined by the level of fecal α-elastase-1. At the beginning of the study and two months after the treatment has started, esophagogastroduodenoscopy + urease test for H. pylori + biopsy from 5 sites with histological examination has been performed. Results: It was found that a significant decrease in lymphohistiocytic infiltration of stomach lining, restoration of the structure of glands which have not undergone atrophy, increased focal hyperplasia (proliferation) of the glandular epithelium as signs of morphological restoration of the epithelium, reduction of epithelial dysplasia signs against the complete absence of positive dynamics of epithelial dysplasia in the group of patients receiving standard treatment of CP and CG, are clear and reliable signs of the effectiveness of vitamin Doctovit in complex therapy of CG associated with H.pylori, which indicate the feasibility of using the medicine to restore SL, which is the basis for effective carcinoprevention. Conclusions: The effectiveness of both treatment complexes in the correction of exocrine insufficiency of the pancreas by the dynamics of fecal α-elastase-1 was proved and which was statistically significantly higher when using the program with the inclusion of Doctovit: respectively 28.12% vs. 20.74% (p&lt; 0.05). The total dynamics of morphological state improvement of stomach lining in the 1st group of patients was 0.9 points against 1.6 points in the 2nd group of patients, which was 17% and 32%, respectively (p &lt;0.05), which activates clinical data on the effectiveness and feasibility of using a combination of dexpanthenol and methylmethionine according to the suggested scheme in the treatment of patients with chronic pancreatitis in comorbidity with H. pylori erosive CG.

Antibacterial Multi-Layered Nanocellulose-Based Patches Loaded with Dexpanthenol for Wound Healing Applications.

Antibacterial multi-layered patches composed of an oxidized bacterial cellulose (OBC) membrane loaded with dexpanthenol (DEX) and coated with several chitosan (CH) and alginate (ALG) layers were fabricated by spin-assisted layer-by-layer (LbL) assembly. Four patches with a distinct number of layers (5, 11, 17, and 21) were prepared. These nanostructured multi-layered patches reveal a thermal stability up to 200 °C, high mechanical performance (Young’s modulus ≥ 4 GPa), and good moisture-uptake capacity (240–250%). Moreover, they inhibited the growth of the skin pathogen Staphylococcus aureus (3.2–log CFU mL−1 reduction) and were non-cytotoxic to human keratinocytes (HaCaT cells). The in vitro release profile of DEX was prolonged with the increasing number of layers, and the time-dependent data imply a diffusion/swelling-controlled drug release mechanism. In addition, the in vitro wound healing assay demonstrated a good cell migration capacity, headed to a complete gap closure after 24 h. These results certify the potential of these multi-layered polysaccharides-based patches toward their application in wound healing.

MALDI mass spectrometry imaging as a complementary analytical method for improved skin distribution analysis of drug molecule and excipients.

In cutaneous drug delivery, it is widely accepted that the choice of excipients affects the delivery of a drug molecule to the skin. MALDI mass spectrometry imaging (MALDI-MSI) is an imaging technique which enables the simultaneous detection of multiple compounds. MALDI-MSI was applied to study the penetration of tofacitinib and excipients in porcine skin from two formulations with sodium lauryl sulphate (SLS) and dexpanthenol (DXP) using Franz diffusion cells. Further, the receptor media was collected for analysis of the permeated amounts of tofacitinib and excipients. The MALDI images showed DXP to be co-localized with tofacitinib in the epidermal and deep dermal region while SLS was distributed in the entire skin compartment. The permeation of tofacitinib for the two formulations was similar after 24h, whereas, the percentage of permeated DXP was higher than for SLS. This study provided an overview of the skin penetration and permeation of drug molecule and excipients. MALDI-MSI showed differences in the DXP and SLS distribution. This indicates that the excipients interact with the skin through different mechanisms. Compound-specific imaging methods such as MALDI-MSI are potential tools to increase the understanding of the complex interplay between skin, excipients and the drug molecule for optimized cutaneous drug delivery.