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羽扇豆醇对7,12-二甲基苯并(a)蒽诱导的口腔癌发生过程中凋亡标志物表达模式的调节作用。

Modulating effect of lupeol on the expression pattern of apoptotic markers in 7, 12-dimethylbenz(a)anthracene induced oral carcinogenesis.

作者信息

Manoharan S, Palanimuthu D, Baskaran N, Silvan S

机构信息

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamilnadu, India.

出版信息

Asian Pac J Cancer Prev. 2012;13(11):5753-7. doi: 10.7314/apjcp.2012.13.11.5753.

DOI:10.7314/apjcp.2012.13.11.5753
PMID:23317251
Abstract

Apoptosis, also known as cell suicide or programmed cell death, removes unwanted and genetically damaged cells from the body. Evasion of apoptosis is one of the major characteristic features of rapidly proliferating tumor cells. Chemopreventive agents inhibit or suppress tumor formation through apoptotic induction in target tissues. The aim of the present study was to investigate the pro-apoptotic potential of lupeol during 7,12-dimethylbenz(a) anthracene (DMBA) induced hamster buccal pouch carcinogenesis. Topical application of 0.5% DMBA three times a week for 14 weeks in the buccal pouches of golden Syrian hamsters resulted in oral squamous cell carcinoma. The expression pattern of apoptotic markers was analyzed using immunohistochemistry (p53, Bcl-2, Bax) and ELISA reader (caspase 3 and 9). In the present study, 100% tumor formation with defects in apoptotic markerexpression pattern was noticed in hamsters treated with DMBA alone. Oral administration of lupeol at a dose of 50 mg/kg bw completely prevented the formation oral tumors as well as decreased the expression p53 and Bcl-2, while increasing the expression of Bax and the activities of caspase 3 and 9. The present study thus indicated that lupeol might inhibit DMBA-induced oral tumor formation through its pro-apoptotic potential in golden Syrian hamsters.

摘要

细胞凋亡,也被称为细胞自杀或程序性细胞死亡,可清除体内不需要的和基因受损的细胞。逃避细胞凋亡是快速增殖的肿瘤细胞的主要特征之一。化学预防剂通过在靶组织中诱导细胞凋亡来抑制或阻止肿瘤形成。本研究的目的是探讨羽扇豆醇在7,12-二甲基苯并(a)蒽(DMBA)诱导的仓鼠颊囊癌变过程中的促凋亡潜力。在金黄叙利亚仓鼠的颊囊中每周三次局部涂抹0.5% DMBA,持续14周,会导致口腔鳞状细胞癌。使用免疫组织化学(p53、Bcl-2、Bax)和酶标仪(caspase 3和9)分析凋亡标志物的表达模式。在本研究中,单独用DMBA处理的仓鼠中观察到100%的肿瘤形成且凋亡标志物表达模式存在缺陷。以50 mg/kg体重的剂量口服羽扇豆醇可完全预防口腔肿瘤的形成,并降低p53和Bcl-2的表达,同时增加Bax的表达以及caspase 3和9的活性。因此,本研究表明羽扇豆醇可能通过其在金黄叙利亚仓鼠中的促凋亡潜力来抑制DMBA诱导的口腔肿瘤形成。

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