Effect of Polygonatum Sibiricum polysaccharides on nude mice model of prostate cancer PC‑3 cells.

The present study aimed to explore the influence of Polygonatum sibiricum polysaccharides (PSP) on the progression of prostate cancer PC‑3 cell xenografts in nude mice, with a specific emphasis on analyzing the regulation of key proteins in the phosphatidylinositol 3‑kinase/protein kinase B (PI3K/Akt) and nuclear factor‑kappa B (NF‑κB) signaling pathways. An androgen‑independent PC‑3 prostate cancer cell line was subcutaneously injected into immunocompromised BALB/c nude mice to establish a xenograft model. The mice were randomly allocated into five groups, each comprising six animals. Drug dosages were determined according to the body surface area ratio between humans and nude mice. The control group was given normal saline, whereas the docetaxel (DTX) group received docetaxel at a dosage of 5 mg/(kg·d). The PSP treatment groups were administered PSP at low [100 mg/(kg x d)], medium [200 mg/(kg x d)], and high [400 mg/(kg x d)] doses. Each treatment was delivered via gavage at a volume of 0.2 ml every other day for a 30‑day period. Tumor volume and body weight were recorded every 3 days to evaluate the effect of PSP on xenograft growth, with tumor size and overall health status serving as the primary assessment criteria. A total of 4 h after drug administration, tumor volume was measured to calculate the tumor inhibition rate. Subsequently, apoptosis in tumor tissues was evaluated using the TUNEL assay. Immunohistochemistry was conducted to detect the expression levels of PI3K, Akt, NF‑κB p65, their phosphorylated forms (p‑PI3K, p‑Akt and p‑NF‑κB p65), and caspase‑3. At the initial stage of establishing the tumor‑bearing nude mouse model of prostate cancer, all groups of nude mice displayed stable mental states, high levels of activity, regular feeding habits and heightened responsiveness to external stimuli. However, as the tumors progressed, a decline in activity, food intake and responsiveness to stimuli was observed across all groups. PSP inhibited the proliferation of PC‑3 cells and induced apoptosis in tumor‑bearing nude mice, presumably by downregulating PI3K, Akt and NF‑κB p65, thereby suppressing the PI3K/Akt and NF‑κB signaling pathways. Simultaneously, PSP upregulated the expression of caspase‑3, which contributed to its antitumor effects in the PC‑3 prostate cancer model.