关键词: 食管肿瘤, 白藜芦醇, 细胞增殖, 细胞凋亡

Abstract: ［Abstract］ Objective〖HTSS〗〓To explore the effects of resveratrol on biological behavior of human esophageal cancer cell EC9706 and its mechanism, and to provide a theoretical basis for the clinical application of resveratrol to prevent or treat esophageal cancer.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓Different concentrations of resveratrol were used to treat EC9706 cells for different time. Cell morphology was observed by inverted phase contrast microscope. Intracellular micromorphological changes were observed under electron microscope. Methylthiazoliltetracolium colorimetric enzyme reactions trace method were used to determinate cell proliferation level. Flow cytometry method was used to detect cell cycle distribution and the expression of apoptosis related protein.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓Resveratrol treatment increased and thickened particles in EC9706 cytoplasm, reduced the cytoplasm, rounded cells and made cells more smaller and the cell shape more diversity, and made the nuclear chromatin condense on the boundary of the nuclear envelope. The electron density was increased, part of the cell membrane bulge was outward and form an acute angle. There was vacuoles degeneration in the cytoplasm. Resveratrol inhibited EC9706 cell proliferation in a dose and timedependent manner. Resveratrol made subdiploid nuclear peak(apoptotic peak) appear before G0/G1  phase in EC9706 cells, and increased the rate of apoptosis together with proportion of G0/G1 phase. In contrast, resveratrol decreased the S and G2/M phase fraction(compared with the control group, P＜001). Resveratrol treatment also decreased expression of bcl2 protein, and increased  expression of bax protein(compared with the control group, P＜001).
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓Resveratrol can inhibit the proliferation and induces apoptosis of EC9706 cells, and make the cell cycle arrest in G0/G1 phase. This effect may be related to apoptosis gene bcl2 and bax.

Key words: esophageal neoplasms; , resveratrol, cell proliferation, apoptosis