Abstract
Abstract Objective Investigation of the anticarcinogenic effects of natural products with low toxicity is very important in the development of new therapeutic strategies against cancer. Ginnalin A (GA) is one of the most important phenolic compounds of Acer genus and its anticancer effect has been shown that in various cancer cell lines. SB203580, a p38 MAPK inhibitor, can inhibit cell proliferation independently of p38 MAPK. The objective of this study was to investigate combination effect of GA and SB203580 on Hep-3B cell line. Material and methods Cell viability was determined by using XTT method after the treatment with GA, SB203580 and combination of both. Anticarcinogenic effects of GA and SB203580 both in single and in combination have been analyzed with Caspase-3 activity assay and expression levels of important genes involved in cell cycle and apoptosis were evaluated by qPCR. Results GA and SB203580 have shown additive effect on Hep-3B cells in the combination inhibited 50% of cell viability. And, SB203580 increased the effect of GA on activation of Caspase-3 and expressions of genes important in apoptosis and cell cycle. Conclusion This study indicates that GA and SB203580 can be an effective for development of new therapeutic strategies in hepatocellular carcinoma.
Highlights
Hepatocellular carcinoma (HCC), the third leading cause of cancer-related death worldwide, is the most commonHasibe Vural et al.: Ginnalin A and SB203580 show additive effect 79 type of primary liver cancer with a rate of 80–90%
The investigation of anticarcinogenic activities of natural products in various cancer cells contributes to the development of new therapeutic strategies against cancer
Ginnalin A (GA) is a phenolic compound found in Acer sp., especially Acer ginnala
Summary
Hasibe Vural et al.: Ginnalin A and SB203580 show additive effect 79 type of primary liver cancer with a rate of 80–90%. It is the fifth most frequent cancer type in men, while is ranked seventh in women [1, 2]. The most important risk factors for HCC are chronic infection with Hepatitis B, C and D viruses, alcohol intake and aflatoxin exposure. The incidence of HCC is high in the East, Southeast and Central Asia and the sub-Saharan Africa where the prevalence of hepatitis infections is high. HCC cases are frequently encountered in South China and sub-Saharan Africa where foods are contaminating with aflatoxin [3,4,5]. Non-alcoholic steatohepatitis, obesity, metabolic diseases such as diabetes and genetic susceptibility can be associated with development of HCC [6]
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