Pterostilbene Inhibits the Proliferation of HCC Cells in vitro by Inducing Autophagy and Apoptosis

碩士 === 中山醫學大學 === 醫學檢驗暨生物技術學系碩士班 === 102 === Petrostilbene is a natural dimethyl analog of resveratrol and found in many grapes and berries, with multiple pharmacologic activities, including anti-inflammation, anti-oxidation and cancer prevention. Many studies showed that pterostilbene can induce ap...

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Bibliographic Details
Main Authors: Chen-Lin Yu, 尤振霖
Other Authors: Hui-Ling Chiou
Format: Others
Language:zh-TW
Published: 2014
Online Access:http://ndltd.ncl.edu.tw/handle/n6d8jb
Description
Summary:碩士 === 中山醫學大學 === 醫學檢驗暨生物技術學系碩士班 === 102 === Petrostilbene is a natural dimethyl analog of resveratrol and found in many grapes and berries, with multiple pharmacologic activities, including anti-inflammation, anti-oxidation and cancer prevention. Many studies showed that pterostilbene can induce apoptosis and autophagy in various cancer cell lines and further inhibit their viability. However, the exact mechanism of pterostilbene-aused growth inhibition in hepato- cellular carcinoma (HCC) cell lines remains unclear. The main goal of this study is to elucidate how pterostilbene inhibit cell proliferation of HCC cells. Results from MTT assay and DAPI staining showed that pterostilbene caused both dose- and time-dependent inhibition of viability of both cells while the morphology of both cells was changed into a more apoptotic fashion. Cell cycle analysis showed that the phase distribution was changed by pterostilbene treatment. However, the expression of caspase 3, 8 and 9 were not affected, indicating that caspase-independent apoptosis may be activated. Meanwhile, results form AO staining showed that pterostilbene treatment can increase the percentage of AVOs positive cells in both dose- and time-dependent manner. Furthermore, the expression level of LC3-II was also increased in both dose- and time-dependent manner by pterostilbene. In summary, pterostilbene inhibit the cellular viabilities of Huh 7 and SK-Hep 1 via cell cycle arrest and the activation of autophagy.