期刊
TUMOR BIOLOGY
卷 36, 期 3, 页码 1763-1771出版社
SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-014-2778-z
关键词
Apoptosis; Angiogenesis; TGF-beta; Akt; Curcumin; Diethylnitrosamine; Hepatocellular carcinoma
类别
资金
- Deanship of Scientific Research, Taibah University, El- Madinah El-Munawarah, Saudi Arabia
- Faculty of Pharmacy Al-azhar University Assuit Branch-Egypt
- Faculty of Pharmacy Minia University, Mina, Egypt
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. In laboratory animal models, diethylnitrosamine (DENA) is a well-known agent that has a potent hepatocarcinogenic effect that is used to induce HCC. As curcumin has a potent anti-inflammatory effect with strong therapeutic potential against a variety of cancers, our present study aims to investigate its curative effects and the possible mechanisms of action against DENA-induced HCC in male rats. Investigation of biochemical and molecular parameters of HCC animal model liver showed an overexpression of TGF-beta and Akt proteins accompanied with a significant reduction of the proapoptotic marker caspase-3. DENA-induced hepatic cellular injury resulted also in a significant increase in liver function marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lipid peroxides in this group. Curcumin treatment partially reversed DENA-induced damage as it reduced the overexpression of the angiogenic and anti-apoptotic factors TGF-beta and Akt and improved caspase-3 expression. Also, it could partially normalize the serum values of liver marker enzymes and lipid peroxidation and improve liver architecture. Curcumin shows a unique chemotherapeutic effect in reversing DENA-induced HCC in rat model. This effect is possibly mediated through its proapoptotic, antioxidant, anti-angiogenic, as well as antimitotic effects. It interferes and modulates cell signaling pathways and hence turns death signals and apoptosis on within tumor cells.
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