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郁郎山多糖在体内外抑制 4T1 乳腺癌细胞增殖并诱导细胞凋亡。

Yulangsan polysaccharide inhibits 4T1 breast cancer cell proliferation and induces apoptosis in vitro and in vivo.

机构信息

Pharmaceutical College, Guangxi Medical University, Nanning, China.

Pharmaceutical College, Guangxi Medical University, Nanning, China.

出版信息

Int J Biol Macromol. 2019 Jan;121:971-980. doi: 10.1016/j.ijbiomac.2018.10.082. Epub 2018 Oct 17.

Abstract

Yulangsan polysaccharide (YLSPS) is derived from the root of Millettia pulchra (Benth.) Kurz var. Recent studies have postulated YLSPS as a regimen for cancer treatment. However, the underlying mechanism anti-breast cancer is still poorly unknown. The aim of this study was to examine the suppressive and apoptosis effect of YLSPS on the growth of breast cancer cell 4T1 and its possible underlying mechanism. In this study, breast cancer cell 4T1 viability and apoptosis were assessed by CCK-8 and flow cytometry, relative quantitative real-time PCR and western blot after treated with drug-serum of YLSPS. Furthermore, therapy experiments were conducted using a Balb/c mouse transplanted tumor model of breast cancer. The number of apoptotic cells and microvascular density (MVD) in the tumor tissues were assessed by TUNEL and CD34 immunostaining. Immunohistochemical assays and ELISA were used to detect the expression of VEGF, Bcl-2, Bax and Caspase-3 in the tissues. The in vitro studies showed that the drug-serum of YLSPS significantly inhibition of proliferation and effectively induced apoptosis of 4T1 cells. Oral administration of YLSPS in the breast cancer models significantly reduced the tumor volume and weight. The enhanced antitumor efficacy was associated with decreased angiogenesis, an enhanced antioxidant capacity, an increased induction of apoptosis and an inhibition of lung metastasis. These findings indicate that YLSPS significantly inhibited mouse breast cancer growth in vitro and in vivo. These data suggest that YLSPS may serve as a potential therapeutic agent for breast cancer.

摘要

云南黄药多糖(YLSPS)来源于密花豆(Benth.) Kurz var.的根。最近的研究假设 YLSPS 是一种癌症治疗方案。然而,其抗乳腺癌的潜在机制仍知之甚少。本研究旨在研究 YLSPS 对乳腺癌细胞 4T1 生长的抑制和凋亡作用及其可能的作用机制。在这项研究中,通过 CCK-8 和流式细胞术、相对定量实时 PCR 和 Western blot 评估 YLSPS 药物血清处理后乳腺癌细胞 4T1 的活力和凋亡情况。此外,还使用 Balb/c 荷瘤乳腺癌小鼠移植瘤模型进行了治疗实验。通过 TUNEL 和 CD34 免疫染色评估肿瘤组织中细胞凋亡和微血管密度(MVD)的数量。免疫组织化学检测和 ELISA 用于检测组织中 VEGF、Bcl-2、Bax 和 Caspase-3 的表达。体外研究表明,YLSPS 药物血清可显著抑制 4T1 细胞的增殖并有效诱导其凋亡。YLSPS 口服给药可显著降低乳腺癌模型中的肿瘤体积和重量。增强的抗肿瘤疗效与血管生成减少、抗氧化能力增强、凋亡诱导增加和肺转移抑制有关。这些发现表明,YLSPS 可显著抑制乳腺癌在体外和体内的生长。这些数据表明,YLSPS 可能是一种治疗乳腺癌的潜在药物。

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