对于癌症患者来说，尼古丁引起的心脏组织损伤是一个问题，但尼古丁经口摄入引起心脏病发病机制尚不明确。本研究旨在研究尼古丁和小球藻对心脏谷胱甘肽稳态、炎症反应、心脏损伤标志物、凋亡蛋白和实验性移植性肿瘤小鼠模型（厄利奇腹水癌；EAC）的组织病理学结果的影响。在体内实验中，雌性瑞士小鼠被分为四组：对照组、小球藻组（100mg/kg）、尼古丁组（100µg/ml/kg）和联合组（尼古丁+小球藻），进行为期40天的实验。此外，使用分子操作环境（MOE）对小球藻成分对caspase-3、TNF-α和IL-1β活性的影响进行探索，以确保其能够对抗尼古丁的毒性效应。结果表明，尼古丁在EAC携带小鼠中引起了显著（P<0.001）的心脏病理学改变，心脏组织酶发生变化。小球藻减弱了尼古丁诱导的心脏谷胱甘肽抑制，抑制了炎症反应，发挥了抗凋亡效应，减轻了心肌损伤标志物，并修复了细胞和组织损伤。此外，分子对接结果显示，小球藻能够与小鼠组织中的白细胞介素-1受体类型1（IL1R1）和肿瘤坏死因子受体超家族成员1A（TNFRSF1A）结合，改善与尼古丁诱导的心脏毒性相关的凋亡和炎症过程。该研究为理解实验性移植性肿瘤中尼古丁引起的心肌损伤提供了模型，强调了小球藻作为一种有益于对尼古丁经口摄入的癌症患者的食品补充剂。版权所有© 2023 Elsevier B.V. 保留所有权利。

Nicotine-induced cardiac tissue damage is a concern for cancer patients, but the exact pathogenesis from nicotine oral exposure is unclear. This study was designed to investigate the impact of nicotine and Chlorella vulgaris (Ch. V) on cardiac glutathione homeostasis, inflammatory response, cardiac damage markers, apoptotic proteins and histopathological findings in an experimentally transplantable neoplasm mouse model (Ehrlich ascites carcinoma; EAC). In the in-vivo experiment, the female Swiss mice were divided into four groups: control, Ch.V (100mg/kg), Nicotine (100µg/ml/kg), and a combination group ( Nocotine+ Ch.V) for 40 days. Furthermore, the effects of C. vulgaris components on caspase-3, TNF-α, and IL-1β activity were explored using Molecular Operating Environment (MOE) docking software to ensure its ability to counteract the toxic effects of nicotine. The results indicated that nicotine has induced significant (P<0.001) cardiopathic alterations in EAC-bearing mice with changes in cardiac tissue enzymes. C. Vulgaris attenuated the nicotine-induced cardiac glutathione inhibition, suppressed the inflammatory response, exerted antiapoptotic effects, mitigated myocardial injury biomarkers, and repaired cellular and tissue damage. Moreover, the molecular docking results revealed the ability of C. vulgaris to bind with interleukin-1 receptor type 1 (IL1R1) and tumor necrosis factor receptor superfamily member 1A (TNFRSF1A) in the mice tissues, ameliorating apoptosis and inflammatory processes associated with nicotine-induced cardiotoxicity. This study provides a model for understanding nicotine-induced myocardial injury during experimentally transplantable neoplasm. It highlights C. vulgaris as a beneficial food supplement for cancer patients exposed to nicotine orally.Copyright © 2023 Elsevier B.V. All rights reserved.