Sürdürülebilir Kalkınma Amaçları

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• MakaleYalnız künye2026Scopus SJRQ2/r/bayburt/11046
  Multi-Pathway Renoprotection by Betanin Against Docetaxel Nephrotoxicity: Modulation of Inflammation, ER Stress, Apoptosis, and Ferroptosis

  Süzen Celbek, Büşra; Akaras, Nurhan; Şimşek, Hasan; Mutlu, Hüseyin; Kızıl, Hamit Emre; Kandemir, Özge; Aygörmez, Serpil; Kandemir, Fatih Mehmet

  Docetaxel (DTX), a cornerstone chemotherapeutic agent, has its clinical utility significantly limited by dose-dependent nephrotoxicity. This study investigated the multi-pathway renoprotective mechanisms of betanin (BTN), a natural antioxidant derived from beetroot, against DTX-induced kidney injury. Male Wistar rats received DTX (30 mg/kg, i.p., single dose) with or without BTN (100 mg/kg/day, p.o.) for 7 days. DTX induced severe renal dysfunction with elevated serum urea and creatinine, and significant oxidative stress characterized by increased MDA and decreased GSH, GPx, SOD, and CAT. Molecular analysis demonstrated widespread upregulation of pro-inflammatory (NF-κB, TNF-α, IL-1β), endoplasmic reticulum stress (PERK, ATF6), pro-apoptotic (Caspase-3, Bax, Apaf-1), and pro-ferroptotic (PTGS2, TfR1) mediators, with concurrent downregulation of protective Bcl-2 and GPx4. Histopathological examination revealed extensive tubular injury, while immunohistochemical analysis showed markedly increased kidney injury marker KIM-1 and decreased aquaporin-1 expression. Remarkably, BTN co-administration significantly attenuated all biochemical, molecular, and structural derangements, restored tissue architecture, and normalized KIM-1 and AQP-1 expression. In conclusion, betanin provides robust, multi-pathway renoprotection against docetaxel-induced nephrotoxicity by concurrently targeting oxidative stress, inflammation, ER stress, apoptosis, and ferroptosis.

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• MakaleYalnız künye2017Scopus SJRQ2/r/bayburt/12443
  Mechanism of capsaicin inhibition of aldose reductase activity

  Alim, Zuhal; Kilinc, Namık; Sengul, Bulent; Beydemir, Sukru

  Aldose reductase (AR) inhibitors play a vital importance as a potential therapeutic and preventive medicine when it comes to hyperglycemia associated diabetic complications. Additionally, capsaicin is used as a food additive and a drug in a number of diverse clinical trials. The aim of this study is to determine the in vitro inhibition behavior of capsaicin on AR enzyme activity, which was obtained from different rat tissues (heart, kidney, liver, and brain). We showed that AR was inhibited by capsaicin in the micromolar range and noncompetitive manner in all of the tissues. Ki values of capsaicin were found to be 8.87, 264, 535, and 597, respectively, in heart AR, kidney AR, liver AR, and brain AR. In conclusion, capsaicin may be an effective molecule when used in low concentrations to prevent diabetic complications associated with the polyol pathway.

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  AtıfScopus21·WoS19·OpenAlex24

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