4.2 Article

Inhibition of U87 Glioblastoma in BALB/c Nude Mice by Serenoa Repens Extract

期刊

INTERNATIONAL JOURNAL OF PHARMACOLOGY
卷 17, 期 5, 页码 271-280

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ASIAN NETWORK SCIENTIFIC INFORMATION-ANSINET
DOI: 10.3923/ijp.2021.271.280

关键词

Glioblastoma; angiogenesis; Chinese medicine; RhoA; serenoa repens; chemotherapy; rho-associated protein kinase

资金

  1. Natural Science Foundation of Liaoning Province of China [2019-ZD-0740]

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The study demonstrated that Serenoa repens extract has anti-tumor effects on glioblastoma in BALB/c nude mice, prolonging survival and reducing tumor infiltration by modulating the NF-kappa B/Cox-2 signaling pathway.
Background and Objective: Glioblastoma is the most common and invasive tumour in human and most glioma is malignant, grows rapidly with a high recurrence rate. This study aimed to study the anti-tumour effect and mechanism of Serenoa repens extract on glioblastoma in BALB/c nude mice. Materials and Methods: Mice were transplanted with U87 glioblastoma cells and assigned to four groups including blank, model, low-dose SR50 and high-dose SR300 groups. Survival test, tumour volume and weight were measured. Natural killer cell activity, spleen index and the CD4(+)/CD8(+) ratio in spleen cells were assayed. Levels of NF-kappa B, Cox-2, MCP-1, Ang-1, annexin II, vimentin and RhoA were determined. Results:Compared to the model group, SR treatment resulted in significantly prolonged survival and a significantly reduced tumour volume and weight in a dose-dependent manner. The spleen index and NK cell activity were lower in the model group compared to that in the control group (p<0.01) and higher with high-dose SR treatment (p<0.05). Ratio of CD4+/CD8+ was increased after SR treatment with a dose-dependent (p<0.05). Level of NF-kappa B, COX-2, MCP-1, RhoA, annexin II and vimentin were significantly decreased, while Ang-1 level was significantly increased by SR treatment compared to the model group (p<0.05). Conclusion: SR could prolong survival and reduce tumour infiltration in U87 tumour-bearing mice by NF-kappa B/Cox-2 signalling.

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