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    Dexpanthenol exhibits antiapoptotic and anti-inflammatory effects against nicotine-induced liver damage by modulating Bax/Bcl-xL, Caspase-3/9, and Akt/NF-?B pathways
    (Wiley, 2024) Uremis, Nuray; Aslan, Meral; Taslidere, Elif; Gurel, Elif
    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-kappa B 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-kappa B, 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-1 beta, MDA, TOS, and oxidative stress index, accompanied by decreased TAS levels. Moreover, nicotine exposure reduced the p-Akt/Akt ratio, increased NF-kappa B, 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-kappa B pathways. Conversely, DEX effectively attenuated nicotine-induced liver injury by modulating apoptosis through NF-kappa B, Caspase-3, Caspase-9, Bax inhibition, and Bcl-xL activation. Chronic nicotine exposure led to oxidative stress, inflammation, and apoptosis, as evidenced by altered protein levels in Bax/Bcl-xL, Caspase-3/9, and Akt/NF-kappa B pathways. Dexpanthenol treatment effectively countered these effects, highlighting its potential as a therapeutic agent for nicotine-related liver injury.image
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    Dexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathway
    (Springer, 2024) Uremis, Muhammed Mehdi; Gurel, Elif; Aslan, Meral; Taslidere, Elif
    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 0.5 mg/kg/day nicotine and/or 500 mg/kg/day DEX for 8 weeks. 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.
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    Effect of perinatal nicotine exposure on oxidative stress and BDNF levels in the brain tissue of offspring rats: The protective role of Vitamin E
    (Churchill Livingstone, 2025) Ozerol, Beyza Guzide; Selcuk, Engin Burak; Gurel, Elif; Uremis, Muhammed Mehdi; Gul, Mehmet; Gul, Semir; Bag, Harika Gozde Gozukara
    Objective: Nicotine, a well-known neurotoxin, induces oxidative stress in fetal tissues, leading to organ damage and fetal growth retardation. This study aims to evaluate oxidative stress parameters in the brain tissue of rat offspring exposed to perinatal nicotine and assess vitamin E's protective effects. Methods: Twenty-five pregnant rats were administered 10 mg/L of nicotine and 300 mg/L of Vitamin E in drinking water starting from the first day of gestation. On gestational day 21, some offspring were euthanized to form the prenatal group. The remaining litters were born naturally, and dams received treatments via drinking water during gestation and lactation (6 weeks). After the lactation period, the pups were weaned and directly treated for an additional 9 weeks, resulting in an overall treatment duration of 15 weeks. Brain tissues were analyzed for MDA, GSH, TOS, TAS, OSI, BDNF, Caspase-3 activity, and histopathological changes. Results: The nicotine-exposed pups exhibited significantly reduced crown-rump length, body mass, and brain mass compared to controls. Nicotine exposure decreased BDNF, GSH, and TAS levels and increased MDA, TOS, and OSI levels. Histopathologically, the nicotine prenatal group showed a significantly higher number of heterochromatic nuclei in brain tissue. Caspase-3 activity did not show a significant increase in nicotine groups compared to the control. Vitamin E supplementation mitigated nicotine-induced brain damage in some measured parameters. Conclusion: Perinatal nicotine exposure induces oxidative damage in the brain tissue of rat offspring, while vitamin E exerts a protective antioxidant effect, preventing nicotine-induced neurotoxicity. Furthermore, the significant reduction in BDNF levels and the increase in heterochromatic nuclei in the nicotine-exposed groups highlight the detrimental impact of nicotine on neurodevelopment, which can be effectively mitigated by vitamin E supplementation.
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    Protective effects of dexpanthenol in carbon tetrachloride-induced myocardial toxicity in rats
    (Churchill Livingstone, 2022) Yildiz, Azibe; Demiralp, Tugba; Vardi, Nigar; Otlu, Gul; Taslidere, Elif; Cirik, Hilal; Gurel, Elif
    Exposure to various organic compounds including several environmental pollutants and drugs can cause cellular damage through the generation of lipid peroxidation products. Carbon tetrachloride (CCl4) is a potent toxic agent that causes peroxidative degeneration in many tissues. Dexpanthenol (Dxp) is a member of the B complex vitamins that exhibits antioxidant effects against lipid peroxidation products. This study was designed to evaluate the cardioprotective effect of Dxp against CCl4-induced myocardial toxicity in rats. Administration of a single dose of CCl4 caused cardiotoxicity by the increase in lipid peroxidation and histopathological changes (cardiomyocytes degeneration, interstitial edema) in the myocardial tissue. Moreover, CCl4 caused a decrease in lactate dehydrogenase (LDH) and troponin-I immunoreactivities, while significantly increasing tumor necrosis factor-alpha (TNF-alpha) and caspase-3 immunoreactivities. On the other hand, administration of Dxp improved biochemical, histopathological, and immunohistochemical parameters compared to the CCl4 treated group. Overall, this study suggests that Dxp is effective in inhibiting CCl4-induced lipid peroxidation, and that administration of Dxp may help prevent CCl4 related inflammation, necrosis, and apoptosis on the cardiac tissue.