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Öğe Anti-inflammatory and antioxidative effects of dexpanthenol on nicotine-induced lung injury in rats(Korean Soc Environmental Risk Assessment & Health Science, 2023) Aslan, Meral; Guerel, Elif; Ueremis, Nuray; Ueremis, Muhammed Mehdi; Taslidere, ElifAim Lung inflammation is a consequence of smoking, tobacco use, nicotine addiction, and the accumulation of toxicants in the body. This study aimed to investigate the association between nicotine-induced lung injury and NF-kappa B activation, as well as changes in redox balance. Furthermore, the protective role of Dexpanthenol against this damage was examined. Method A total of 32 male rats were divided into four groups: Control, DEX, Nicotine, and Nicotine + DEX. Nicotine (0.5 mg/kg/day) and Dexpanthenol (500 mg/kg/day) were administered intraperitoneally. Subsequently, the levels of nuclear and cytoplasmic NF-kappa B in lung tissue were analyzed. Inflammation and oxidative stress markers and histopathological evaluations of the lung tissue were conducted. Results Nicotine administration resulted in increased levels of tissue MDA and TOS, as well as decreased levels of GSH-Px, GSH, GST, SOD, and TAS. Additionally, nicotine administration led to elevated nuclear expression of NF-kappa B protein, IL-1 beta, IL-6 proinflammatory cytokine levels, and Galectin-3 levels, which modulate cytokine release. Moreover, histopathological examinations revealed a higher population of diffuse lymphocytes and macrophages, indicating increased lung inflammation. Dexpanthenol administration ameliorated these adverse effects of nicotine and reduced them to levels comparable to the control group. Conclusion Nicotine-induced lung injury promoted oxidative stress and inflammation through modulation of NF-kappa B's nuclear translocation. Dexpanthenol, on the other hand, may serve as a dietary supplement to mitigate lung inflammation caused by smoking and tobacco use.Öğe 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, ElifChronic 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.imageÖğe 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, ElifDexpanthenol (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.Öğe Nikotin ile oluşturulmuş deneysel akciğer toksisitesi modelinde dekspantenolün antioksidan ve antiinflamatuar etkisinin araştırılması(İnönü Üniversitesi, 2022) Aslan, MeralAmaç: Nikotinin akciğer dokusunda oluşturduğu hasarı onarımında, Dekspantenolün antiinflamatuar ve antioksidan etkilerinin araştırılması. Materyal ve metot: İnönü Üniversitesi Deney Hayvanları Üretim ve Araştırma Merkezi'nden tedarik edilen, 250-300 gram ağırlığında 32 adet Spraque Dawley cinsi erkek ratlar kullanıldı. Ratlar rastgele 4 eşit gruba ayrıldı; Kontrol grubu, nikotin grubu, dekspantenol grubu, dekspantenol + nikotin grubu olarak ayrıldı. 8 hafta boyunca Nikotin ve Dekspantenol gruplarına intraperitonal olarak uygulama yapıldı (Nikotin 0.5mg/kg-gün, Dekspantenol 500 mg/kg/gün). 8 haftanın sonunda ratların akciğer doku ve kan örnekleri alınarak, biyokimyasal ve histolojik incelemeler yapıldı. Bulgular: Nikotin uygulanması, ratların akciğer dokusunda oksidatif stres parametrelerini arttırmış MDA, TOS, OSİ (P=0.002), antioksidan parametrelerini düşürmüştür (CAT, GSH-Px, SOD, GSH, GST). Bu durum histopatolojik durumlara yol açarak, akciğer dokusunda inflamasyona neden olmuş ve inflamasyon faktörlerinden, IL-1β ve IL-6 değerlerinde artışa sebep olmuştur. Dekspantenol uygulaması akciğer dokusunda antioksidan parametreleri düzeyini arttırırken, oksidan (MDA) ve serum inflamasyon değerlerinde (IL-1β ve IL-6) düşüşlere neden olmuştur. Nikotin ile dekspantenol uygulaması nikotinin biyokimyasal ve histopatolojik etkilerini azaltmaya çalışmıştır. Sonuç: Nikotin akciğer dokusunda hücre harabiyetini oluşturarak, toksisiteye neden olmuş beraberinde inflamasyonlar oluşmuştur. Dekspantenol ise antioksidan ve antiinflamatuar etki göstermiştir. Nikotinin toksik etkilerini tedavi etmek için tedavi protokolüne dekspantenol eklenebilir. Anahtar Kelimeler: Akciğer, Dekspantenol, Histopatoloji, Nikotin, Oksidatif Stres Parametreleri, Rat
