Resveratrol induces apoptosis in human primary gastric carcinoma cells
- VernacularTitle:白藜芦醇诱导胃癌原代细胞凋亡
- Author:
Haibo ZHOU
;
Yun YAN
;
Jianting CAI
;
Qin DU
;
Jinming CHEN
- Publication Type:Journal Article
- Keywords:
Resveratrol;
Stomach neoplasms;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2005;21(7):1340-1344
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the apoptosis in primary gastric 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 gowth inhibitory rate. Transmission electron microscopy and TUNEL staining were used to quantitatively and qualitively detect the apoptosis of primary gastric cancer cells before and after the resveratrol treatment. Immunohistochemical staining and RT - PCR was used to detect the expression of apoptosis - regulated gene bcl - 2 and bax. RESULTS: Resveratrol inhibited the growth of primary gastric cancer cells in a dose - and time - dependent manner. Resveratrol induced primary gastric cancer cells to undergo apoptosis with typically apoptotic characteristics. TUNEL assay showed that after the treatment of primary gastric cancer cells with resveratrol for 24, 48, 72, 96 hours, the apoptotic indexs were 4.93% ± 0.19%, 16.74% ± 0.43%, 27.88% ±0.36%, 36.84% ± 1.07 % respectively. Immunohistochemical staining showed that after the treatment of primary gastric cancer cells with resveratrol for 24, 48, 72, 96 hours, the positive rates of Bcl - 2 proteins were 20.68% ± 0.49%, 10.84% ±0.33%, 6.80% ± 0.34%, 3.91% ± 0.15% and the positive rates of Bax proteins were 19.79% ± 0.98%, 30.74% ±0.85%, 40.14% ± 1.17%, 60.08% ± 1.64%. After exposed to resveratrol for 24 h, 48 h, 72 h and 96 h, the density of bcl- 2 mRNA decreased progressively with elongation of time and the density of bax mRNA increased progressively with elongation of time by RT- PCR. CONCLUSION: Resveratrol is able to induce the apoptosis in primary gastric cancer. This apoptosis may be mediated by down- regulation of Bcl- 2 and up- regulation of Bax.
