BMC Cancer. 2025 Nov 25. doi: 10.1186/s12885-025-15279-2. Online ahead of print.
ABSTRACT
The anticancer activity of sulforaphane (SFN) involves multiple signaling pathways, but its mechanism against Ehrlich Ascites Carcinoma (EAC) in mice remains unclear. This study evaluated the antitumor efficacy of SFN-loaded nanoliposomes (SFN-NLPs). Ninety female Swiss albino mice were allocated into six groups: (1) untreated control, (2) SFN alone (50 mg/kg/day, orally), (3) SFN-NLPs alone (50 mg/kg/day, orally), (4) EAC-bearing mice (2.5 ร 10โถ cells, intraperitoneally), (5) EAC + SFN, and (6) EAC + SFN-NLPs. with treatment lasting 20 days in tumor-bearing groups. SFN-NLPs significantly reduced EAC tumor volume, viable cell count, and tumor marker levels, while prolonging survival more effectively than free SFN. SFN-NLPs modulated key molecular pathways by suppressing inflammatory gene expression (NF-ฮบB, COX-2) and shifting the balance toward apoptosis via upregulation of TP53 and Bax and concomitant downregulation of Bcl-2. Regarding liver integrity, SFN-NLPs significantly reduced DNA fragmentation and hepatic oxidative stress, while modulating systemic inflammation through reductions in total leukocyte count, TNF-ฮฑ, and C-reactive protein. In addition, SFN-NLPs conferred superior protection against both histopathological and ultrastructural liver damage. Furthermore, molecular docking analysis suggested plausible interactions of SFN with proteins associated with antioxidant defense, inflammation regulation, and apoptosis, indicating a potential modulatory role. In conclusion, nanoformulated SFN enhances stability, augments efficacy, and facilitates sustained release and bioavailability, thereby strengthening its antitumor, anti-inflammatory, antioxidant, and pro-apoptotic effects in EAC-bearing mice. These findings highlight the potential of SFN-NLPs to suppress tumor growth by modulating inflammatory and apoptotic gene expression while preserving liver integrity.
PMID:41291551 | DOI:10.1186/s12885-025-15279-2