Effect of Semecarpus anacardium nut extract on ECM and proteases in mammary carcinoma rats

被引:10
作者
Mathivadhani, P.
Shanthi, P.
Sachdanandam, P.
机构
[1] Univ Madras, Dept Med Biochem, Dr ALM Post Grad, Inst Basic Med Sci, Madras 600113, Tamil Nadu, India
[2] Univ Madras, Dept Pathol, Dr ALM Post Grad, Inst Basic Med Sci, Madras, Tamil Nadu, India
关键词
Semecarpus anacardium; breast cancer; proteases; ECM degradation;
D O I
10.1016/j.vph.2006.12.004
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The early stages of invasion are characterized by the extracellular proteolysis and the accumulation of specialized extracellular matrix (ECM) scaffold, that are responsible for the development of vascular bed, endothelial cell proliferation and invasion of tumour cells. The ground substance of provisional matrix consists of collagen, clastin, glycoaminoglycans and proteoglycans that facilitate the interaction of tumour cells with the host environment. In the present work, we have studied the influence of Semecarpus anacardium nut milk extract on localized differentials of ECM component and proteases involved in matrix metabolism of tumour tissue. Mammary carcinoma was induced in Sprague Dawley rats with 7,12, dimethyl benz(a)anthracene and treated with S. anacardium nut milk extract administered orally for 14 days. The altered amount of ECM components in tumour tissues was almost reverted back to normal level in the drug treated animals. The activities of reported proteases and glycohydrolases were also decreased on treatment with S. anacardium nut milk extract indicating decreased turnover of the matrix. Also, the factors associated with the matrix turnover and expression of MMP-1, MMP-2, MMP-3, TIMP-1 and TIMP-2 were restored back to near normal values. The stabilization of the ECM with the decreased activity of proteases might inhibit the epithelial-endothelial interaction and tumour cell migration thus, preventing the adjacent invasion and tumour growth and might be regarded as antineoplastic agent which demands further studies. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:419 / 426
页数:8
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