Tirgar Pravin, Vekaria Mrudul, Raval Keval
School of Pharmacy, RK University, Rajkot, Gujarat, India.
PhaseCare Research, Ahmedabad, Gujarat, India.
Naunyn Schmiedebergs Arch Pharmacol. 2025 Feb;398(2):1825-1839. doi: 10.1007/s00210-024-03389-w. Epub 2024 Aug 23.
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.
研究羽扇豆醇对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35mg/kg DMBA诱导乳腺癌。将动物分为六组。三组给予羽扇豆醇（50mg/kg、100mg/kg和200mg/kg），并进行为期20周的每日治疗（包括2周的预处理）。标准对照组每周两次给予阿霉素（4mg/kg），共20周。疾病对照组（DC）和正常对照组（NC）每日给予生理盐水治疗。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位移蛋白/切割同源框（CUP/Cux）和支架/基质附着区域结合蛋白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。
与DC组相比，羽扇豆醇治疗的动物肿瘤生长显著降低（P值<0.01）。与DC组相比，羽扇豆醇显著（P值<0.01）调节氧化应激参数、生化参数和炎症参数的水平。羽扇豆醇治疗显著（P值<0.001）调节SMAR1和CDP/Cux的表达水平。在羽扇豆醇组中，观察到ER、PR和HER2表达的IHC评分显著降低。
羽扇豆醇在动物中对DMBA诱导的乳腺癌具有化学保护活性，可能是通过调节SMAR1和CDP/Cux基因表达以及降低ER、PR和HER2表达水平来实现的。
