Caffeine mitigates tamoxifen-induced fatty liver in Wistar rats.

Acta cirurgica brasileira Pub Date : 2024-09-30 eCollection Date: 2024-01-01 DOI:10.1590/acb396924
Yasin Sezgin, Ejder Saylav Bora, Duygu Burcu Arda, Yiğit Uyanikgil, Oytun Erbaş
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Abstract

Purpose: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats.

Methods: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration.

Results: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001).

Conclusions: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.

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咖啡因可减轻他莫昔芬诱发的 Wistar 大鼠脂肪肝。
目的:他莫昔芬是一种广泛用于治疗乳腺癌的药物,它对肝脏有不良影响,包括导致脂肪肝。本研究旨在探讨咖啡因对他莫昔芬诱发的 Wistar 大鼠脂肪肝的潜在保护作用:方法:大鼠分为正常对照组、他莫昔芬+生理盐水组和他莫昔芬+咖啡因组。评估血浆样本中与氧化应激、炎症、肝功能和细胞损伤相关的生化指标。此外,还对肝脏组织病理学进行了检查,以量化脂肪浸润的程度:结果:与正常对照组相比,他莫昔芬+生理盐水组的血浆丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、丙氨酸氨基转移酶(ALT)、细胞角蛋白18和可溶性ST2水平升高,表明氧化应激、炎症和肝损伤加重(P < 0.01)。此外,组织病理学检查显示脂肪浸润显著增加(p < 0.001)。然而,在他莫昔芬+咖啡因组,这些标记物明显减少(p < 0.05,p < 0.01),脂肪浸润明显减轻(p < 0.001):结论:研究结果表明,咖啡因能减轻氧化应激、炎症、肝损伤和细胞损伤,从而减轻他莫昔芬诱发的大鼠脂肪肝。组织病理学证据进一步证实了咖啡因的保护作用。这项研究强调了咖啡因作为一种治疗干预措施,对抗他莫昔芬诱发的肝脏并发症的潜力,有助于优化乳腺癌治疗策略。
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