为了研究 karanjin 对 7,12-二甲基苯并 (α) 蒽 (DMBA) 诱导的乳腺癌的化学保护潜力。本研究使用了 36 只雌性大鼠。通过皮下注射 35 毫克/千克 DMBA 诱发乳腺癌。将动物分为六组。三组被分配为 karanjin（50 mg/kg、100 mg/kg 和 200 mg/kg），并接受为期 20 周的每日治疗（包括 2 周作为预处理）。标准对照组每周两次服用阿霉素（4 毫克/公斤），持续 20 周。疾病对照（DC）组和正常对照（NC）组每天接受生理盐水治疗。治疗后，评估氧化应激参数、生化参数和炎症参数。通过基因表达分析测量 CCAAT 置换蛋白/切割同源盒 (CUP/Cux) 和支架/基质附着区结合蛋白 1 (SMAR1) 的表达水平。进行免疫组织化学 (IHC) 分析以评估雌激素受体 (ER)、孕激素受体 (PR) 和人表皮生长因子受体 2 (HER2) 的表达。karanjin 中的肿瘤生长显着减少（P 值 < 0.01）与DC组相比，治疗的动物。与DC组相比，Karanjin显着（P值<0.01）调节氧化应激参数、生化参数和炎症参数的水平。 Karanjin 处理显着（P 值 < 0.001）调节 SMAR1 和 CDP/Cux 的表达水平。在 karanjin 组中观察到 ER、PR 和 HER2 表达的 IHC 评分显着降低。Karanjin 通过调节 SMAR1 和 CDP/Cux 基因表达以及减少 ER、PR 的表达，对 DMBA 诱导的动物乳腺癌具有化学保护活性。和 HER2 表达水平。© 2024。作者获得 Springer-Verlag GmbH 德国（Springer Nature 旗下公司）的独家许可。

To investigate the chemoprotective potential of karanjin against 7,12-dimethylbenz(α)anthracene (DMBA)-induced breast cancer.Thirty-six female rats were utilized for the study. Breast cancer was induced through a subcutaneous injection of 35 mg/kg DMBA. The animals were allocated to six groups. Three groups were allocated for karanjin (50 mg/kg, 100 mg/kg, and 200 mg/kg), and received daily treatment for 20 weeks (including 2 weeks as pre-treatment). Doxorubicin (4 mg/kg) was administered to the standard control group twice a week for 20 weeks. The disease control (DC) and normal control (NC) groups received daily treatment with saline. After the treatment, oxidative stress parameters, biochemical parameters, and inflammatory parameters were estimated. CCAAT-displacement protein/cut homeobox (CUP/Cux) and scaffold/matrix attachment region binding protein 1 (SMAR1) expression levels were measured through gene expression analysis. Immunohistochemical (IHC) analysis was performed to estimate the expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2).Tumor growth reduced significantly (P-value < 0.01) in karanjin-treated animals compared to the DC group. Karanjin significantly (P-value < 0.01) regulated the levels of oxidative stress parameters, biochemical parameters, and inflammatory parameters compared to the DC group. Karanjin treatment significantly (P-value < 0.001) regulated the expression levels of SMAR1 and CDP/Cux. A notable reduction in the IHC scores was observed for ER, PR, and HER2 expression in karanjin groups.Karanjin demonstrated chemoprotective activity against DMBA-induced breast cancer in animals potentially through modulation of SMAR1 and CDP/Cux gene expression and reduction of ER, PR and HER2 expression levels.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.