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

Üremiş, Muhammed Mehdi; Gürel, Elif; Aslan, Meral; Taşlıdere, Elif

doi:10.1007/s00210-023-02671-7

Cited by 2 publications

(2 citation statements)

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“…DEX also decreases inflammatory cytokine levels and reactive oxygen species (ROS) accumulation, demonstrating its protective effects. [25,26] In vivo studies have highlighted DEX's contribution to tissue regeneration, increasing antioxidant defense, and promoting cellular healing by regulating inflammation processes. [19,27] This study aims to investigate DEX's protective effect against nicotine-induced liver damage, focusing on inflammatory and apoptotic mechanisms such as Akt/NF-κB, Bax/Bcl-xL, and Caspase-3/9.…”

Section: Introductionmentioning

confidence: 99%

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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‐κB pathways

Üremiş,

Aslan,

Taşlidere

et al. 2024

J Biochem & Molecular Tox

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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.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Üremiş,

Aslan,

Taşlidere

et al. 2024

J Biochem & Molecular Tox

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Effects of ethyl 7-hydroxy-2-imino-2H-chromene-3-carboxylate, a synthesized coumarin derivative, on bisphenol A-induced kidney toxicity

Akgül,

Üremiş,

Üremiş

et al. 2024

Adıyaman Üniversitesi Sağlık Bilimleri Dergisi

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Aim: In this study, it was aimed to investigate the protective effect of the synthesized coumarin ethyl 7-hydroxy-2-imino-2H-chromene-3 carboxylate (CM) against the renal toxicity of Bisphenol A (BPA). Materials and Methods: The CM molecule was synthesised through the reaction between 2,4-dihydroxybenzaldehyde and ethyl cyanoacetate. Experiment was conducted in four groups of rats: control, BPA, CM, and BPA+CM. Total Antioxidant Status (TAS), Total Oxidant Status (TOS), and Malondialdehyde (MDA) levels in kidney tissue were evaluated. serum samples were analyzed for Total-Native thiol and kidney function test parameters. Results: The BPA-treated group exhibited significant decreases in TAS and thiol levels, increases in TOS and MDA levels. However, these side effects were significantly reduced with CM. Conclusion: results obtained in this study indicate that CM molecule has a protective effect against BPA induced kidney toxicity.

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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

Cited by 2 publications

References 46 publications

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

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

Effects of ethyl 7-hydroxy-2-imino-2H-chromene-3-carboxylate, a synthesized coumarin derivative, on bisphenol A-induced kidney toxicity

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