Sezgin Yasin, Bora Ejder Saylav, Arda Duygu Burcu, Uyanikgil Yiğit, Erbaş Oytun
Yüzüncü Yıl University - Faculty of Medicine - Clinic of Medical Oncology - Van - Turkey.
İzmir Katip Çelebi University - Faculty of Medicine - Department of Emergency Medicine - Izmir - Turkey.
Acta Cir Bras. 2024 Sep 30;39:e396924. doi: 10.1590/acb396924. eCollection 2024.
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.
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.
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).
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.
他莫昔芬是一种广泛用于治疗乳腺癌的药物，与肝脏不良反应有关，包括脂肪肝的发生。本研究旨在探讨咖啡因对他莫昔芬诱导的Wistar大鼠脂肪肝的潜在保护作用。
将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标志物。此外，检查肝脏组织病理学以量化脂肪浸润程度。
与正常对照组相比，他莫昔芬+生理盐水组血浆丙二醛（MDA）、肿瘤坏死因子-α（TNF-α）、丙氨酸转氨酶（ALT）、细胞角蛋白18和可溶性ST2水平升高，表明氧化应激、炎症和肝损伤增加（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+咖啡因组中，这些标志物明显降低（p<0.05，p<0.01），脂肪浸润明显减轻（p<0.001）。
研究结果表明，给予咖啡因可通过改善氧化应激、炎症、肝损伤和细胞损伤来减轻他莫昔芬诱导的大鼠脂肪肝。组织病理学证据进一步支持了咖啡因的保护作用。本研究强调了咖啡因作为一种治疗干预措施来对抗他莫昔芬诱导的肝脏并发症的潜力，有助于优化乳腺癌治疗策略。
