Resveratrol induces apoptosis in human esophageal carcinoma cells
Autor: | Ya-Ni Sun, Yun Yan, Hai-Bo Zhou, Ju-Ren Zhu |
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Rok vydání: | 2003 |
Předmět: |
TUNEL assay
Esophageal Neoplasms Esophageal Cancer Cell growth Carcinoma Gastroenterology Apoptosis General Medicine Biology Resveratrol Apoptotic body Molecular biology Antineoplastic Agents Phytogenic Chromatin chemistry.chemical_compound chemistry Cell culture Stilbenes Tumor Cells Cultured Humans MTT assay |
Zdroj: | World journal of gastroenterology. 9(3) |
ISSN: | 1007-9327 |
Popis: | AIM: To investigate the apoptosis in esophageal cancer cells induced by resveratrol, and the relation between this apoptosis and expression of Bcl-2 and Bax. METHODS: In in vitro experiments, MTT assay was used to determine the cell growth inhibitory rate. Transmission electron microscope and TUNEL staining method were used to quantitatively and qualitively detect the apoptosis status of esophageal cancer cell line EC-9706 before and after the resveratrol treatment. Immunohistochemical staining was used to detect the expression of apoptosis-regulated gene Bcl-2 and Bax. RESULTS: Resveratrol inhibited the growth of esophageal cancer cell line EC-9706 in a dose-and time-dependent manner. Resveratrol induced EC-9706 cells to undergo apoptosis with typically apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation and apoptotic body formation. TUNEL assay showed that after the treatment of EC-9706 cells with resveratrol (10 mmol·L-1) for 24 to 96 hs, the AIs were apparently increased with treated time (P < 0.05). Immunohistochemical staining showed that after the treatment of EC-9706 cells with resveratrol (10 mmol·L-1) for 24 to 96 hs, the PRs of Bcl-2 proteins were apparently reduced with treated time (P < 0.05) and the PRs of Bax proteins were apparently increased with treated time (P < 0.05). CONCLUSION: Resveratrol is able to induce the apoptosis in esophageal cancer. This apoptosis may be mediated by down-regulating the apoptosis-regulated gene Bcl-2 and up-regulating the expression of apoptosis-regulated gene bax. |
Databáze: | OpenAIRE |
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