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- MakaleAçık Erişim2025Scopus SJRQ1The Protective Effect of Boric Acid Against High Fructose-Induced Liver and Kidney Damage in Rats
Yüksel, Duygu; Başeğmez, Mehmet; Kan, Fahriye
This study aimed to determine the protective role of boric acid (BA) in high fructose (HF)-induced liver and kidney toxicity in a young rat model. High-fructose consumption causes serious damage to liver and kidney tissue in healthy individuals and contributes to the emergence of various metabolic diseases. Thirty-two healthy female Wistar albino rats (250–300 g weight and 3–4 months) were randomly distributed into four equal groups (n = 8): control, high fructose % 20 (HF), boric acid 20 mg/kg (BA), and HF + BA. High fructose was freshly prepared and administered to the rats as 20 g of d-fructose dissolved in 100 mL of tap water daily for a duration of 30 days. Boric acid (20 mg/kg) was administered through gastric gavage throughout the 30-day study period. At the end of study, blood, liver, and kidney were collected from rats. The results indicated that high fructose induced increased glucose, total cholesterol, triglyceride, and urea levels in rat serum. Boric acid administration significantly decreased glucose, total cholesterol, triglyceride, and urea levels in HF + BA groups. The results indicated that high fructose-induced oxidative stress by increasing the level of MDA and by decreasing GSH levels, and CAT activity in the liver and kidney of rats. However, oral BA administration significantly decreased MDA levels and increased GSH levels, and CAT activity (p < 0.05). Furthermore, BA significantly reduced high fructose-induced histopathological and Immunohistochemistry alteration in the liver and kidney tissues. In conclusion, BA may prevent the oxidative imbalance and histopathological and immunohistochemical damage caused by high fructose in liver and kidney tissues in rats.
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İncele - MakaleYayıncıda açık erişim2025Scopus SJRQ2Could Different Doses of Dexmedetomidine Be as Effective as Amifostine Against Radiotherapy-Induced Liver Injury in Rats? Evidence from Mitotic, Apoptotic, Oxidative, and Neurogenic Insights
Beyazal Polat, Hatice; Yilmaz, Hamit; Demir, Kasim; Kilinc, Kagan; Gülhan, Belemir; Rakici, Sema Yilmaz; Tumkaya, Levent
Background/Objectives: Radiotherapy (RT) induces oxidative stress and structural damage in solid tissues, including the liver. This study aimed to investigate the histological and immunohistochemical effects of dexmedetomidine (DEX) and amifostine on their potential protective and regenerative properties against liver injury induced by radiation therapy. Methods: This study consisted of five randomized groups: control, RT, RT-D100, RT-D200, and RT-A (Amifostine). A total of 100 mu g/kg DEX, 200 mu g/kg DEX, and 200 mu g/kg amifostine were administered before radiotherapy as per the experimental design. After RT, liver specimens were analyzed for histological alterations, including periportal and perisinusoidal fibrosis, vacuolization, and pyknotic nuclei. Furthermore, immunohistochemistry investigations were conducted to evaluate apoptosis, mitosis, oxidative stress, and neural regeneration in non-neuronal liver tissue following radiotherapy and subsequent treatment. Results: The control group's liver tissue exhibited standard histological architecture, whereas the RT group displayed severe cellular degeneration, periportal and perisinusoidal fibrosis, cytoplasmic vacuolization, and an increase in pyknotic nuclei. The apoptotic index was markedly reduced in the RT-D100 and RT-D200 groups relative to the RT group. Furthermore, caspase-3 immunoactivity was negligible in the control group, while a significant increase was observed in the RT group. The administration of amifostine significantly increased GAP-43 levels. Conclusions: DEX mitigates RT-induced hepatic injury chiefly through antioxidant and anti-apoptotic pathways, whereas amifostine promotes hepatic regeneration by modulating GAP-43.