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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

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Abstract

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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Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Acknowledgements

The authors are very thankful to Bayer Turk Chemical Industry for supplying the Dexpanthenol substance for the proposed research works.

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MMÜ carried out the biochemical analysis, data analysis and wrote the paper; EG conceived the study and designed experiments; MA conducted the biochemical experiments; ET conducted histochemical experiments. All authors read and approved the final manuscript. The authors declare that all data were generated in-house and that no paper mill was used.

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Correspondence to Muhammed Mehdi Üremiş.

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The study obtained ethical approval from the Inonu University Faculty of Medicine Experimental Animals Ethics Committee (Decision No: 2021/3–2), ensuring compliance with ethical guidelines and regulations.

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Üremiş, M.M., Gürel, E., Aslan, M. et al. Dexpanthenol protects against nicotine-induced kidney injury by reducing oxidative stress and apoptosis through activation of the AKT/Nrf2/HO-1 pathway. Naunyn-Schmiedeberg's Arch Pharmacol 397, 1105–1114 (2024). https://doi.org/10.1007/s00210-023-02671-7

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