Antiproliferative potential of gallic acid against diethylnitrosamine-induced rat hepatocellular carcinoma

被引：87

作者：

Jagan, Sundaram ^{[1
]}

Ramakrishnan, Gopalakrishnan ^{[1
]}

Anandakumar, Pandi ^{[1
]}

Kamaraj, Sattu ^{[1
]}

Devaki, Thiruvengadam ^{[1
]}

机构：

[1] Univ Madras, Dept Biochem, Madras 600025, Tamil Nadu, India

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2008年 / 319卷 / 1-2期

关键词：

Gallic acid; Diethylnitrosamine; Hepatocellular carcinoma; Tumor markers; Proliferation; PCNA;

D O I：

10.1007/s11010-008-9876-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

One of the focuses in current cancer chemoprevention studies is the search for nontoxic chemopreventive agents that inhibit the initiation of malignant transformation. Cancer biomarkers are quantifiable molecules involved in the physiologic or pathologic events occurring between exposure to carcinogens and the development, progression of cancer. Biomarkers may be the consequence of a continuous process, such as increased cell mass, or a discrete event, such as genetic mutation. Analysis of tumor markers can be used as an indicator of tumor response to therapy. Gallic acid is a naturally available polyphenol, possess strong antioxidant activity with a capacity to inhibit the formation of tumors in several cancer models. In the present study, we investigated the antiproliferative effect of gallic acid during diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) in male wistar albino rats. DEN treatment resulted in increased levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, acid phosphatase, lactate dehydrogenase, gamma-glutamyltransferase, 5'-nucleotidase, bilirubin, alpha-fetoprotein, carcinoembryonic antigen, argyophillic nucleolar organizing regions, and proliferating cell nuclear antigen. Gallic acid treatment significantly attenuated these alterations and decreased the levels of AgNORs and PCNA. These finding suggests that gallic acid is a potent antiproliferative agent against DEN-induced HCC.

引用

页码：51 / 59

页数：9

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