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Resveratrol is a phytoalexin with resistant pathogens in plants; resveratrol has anti-tumor effects in animal body. 2-4/10 people, the incidence rate of leukemia in China's population is one of the major diseases of cancer deaths. Ordinary and conventional treatment, the majority of tumors, including leukemia treatment is not ideal. Attract many scholars note that the natural food ingredients can inhibit, delay or reverse tumor initiation and development, resveratrol is a natural plant polyphenols in grapes (including wine), and peanuts, and other plants there. Resveratrol with a variety of diseases and tumor suppression, delay and reversal. Recent studies have shown that resveratrol has the chemical protective effects, and can induce cell cycle inhibition and apoptosis. This study resveratrol acute T lymphoblastoid cell leukemia Jurkat cells and Burkitt B lymphoma Raji cell proliferation inhibition, apoptosis induction, to investigate the induction of tumor cell death pathways, analysis of the possible role of resveratrol in the treatment of leukemia. Studies have shown that resveratrol can inhibit the proliferation of Jurkat cells, a dose-and time-dependent inhibition. Visible morphological changes of apoptosis self-12h, 0.16mmol / L treated cells, more pronounced with time; Hoechest 33258 staining visible The median inhibitory amount of processing most of the 24h group nuclei were uniform pale blue fluorescence, a small part of the nucleus The bright blue, with the incubation time, a gradual increase in the number of bright blue staining cells. Wrigh-Giemsa staining and transmission electron microscope visible some cell shrinkage, chromatin condensation and margination phenomenon. Agarose gel electrophoresis, 0.16mmol / L resveratrol for 24h, 36h 48 hours after the visible DNA \Flow cytometry for 48h, various concentration treatments can be detected the hypodiploid peaks, 0.015,0.03,0.06 mmol / L resveratrol treatment group ratio of apoptotic cells were 5.49%, 6.78%, 12.01%, the control group was 2.05%; resveratrol caused Jurkat cells s arrest, 0.06mmol / L resveratrol 48h after treatment, 62.5% of the cells were arrested at cells the S phase of the cycle. Resveratrol inhibits proliferation of Raji cells in a dose-and time-dependent. However, most of Raji cells to resveratrol treatment did not show the typical characteristics of apoptosis. Inhibition with half the amount of resveratrol (0.22mmol / L) treatment Raji cells 48h, no cytoplasmic significantly concentrated, nuclear fragmentation, chromosome marginalization of the typical characteristics of apoptosis; agarose gel electrophoresis, 0.22mmol / L resveratrol for 12h, 24h, 36h after 48 hours showed no DNA \The characteristics of electron microscopy is able to accurately determine the type of cell death, a detection method, to be able to distinguish between the possibility of death. Electron microscopy showed that resveratrol treatment after 48h, Raji cells appears a lot of autophagy vesicles. Autophagy vesicles containing the degradation of organelles and cytoplasmic components. These data indicate that, Raji cells undergo cell death autophagy. MDC is a with self swallowed the body selective binding fluorescent substances used to obtain supporting evidence supports resveratrol triggers autophagy conclusion. Raji cells treated with resveratrol, MDC staining, fluorescence microscopy, and results show that the massive fluorescent structure of the treated cells point significantly increased. Jurkat cells were used as a control, the untreated Raji cells and resveratrol treatment only low levels of fluorescence. Western blotting analysis showed that resveratrol treatment Raji cells, can not lead to the activation of caspase-3, resveratrol through caspase-independent-dependent pathway Raji cells induced autophagy death cathepsin D (Cathepsin D, Cath D) species lysosomal proteases play an important role in protein degradation and oxidative stress, cytokines, or caused by aging of the apoptotic process. Therefore, the present study was to investigate the role of cathepsin D in the resveratrol-induced apoptosis in Jurkat cells and Raji cell death is autophagy. Raji cells treated with resveratrol (half inhibitory amount: 0.22mmol / L) and Jurkat cells (median inhibitory amount: 0.16 mmol / L), 12h, 24h, and 48h, respectively, the cells were harvested by Western blot analysis. 32kDa the active Cath D component in Jurkat cells, but compared with the control group, did not change significantly. In Raji cells, the activity of Cath D component of 32kDa, with the treatment time is reduced. May be due to the decrease in Cath D, in the emergence of drug-resistant tumor cells for chemical drugs induce tumor cell apoptosis, mitochondrial damage smaller, through autophagy pathway induces cell death. Conclusion: resveratrol can inhibit Jurkat cells, causing the S phase of the cell cycle arrest and induction of apoptosis. 2 resveratrol can inhibit the proliferation of Raji cells and induced autophagy. The 3 Resveratraol both caspase-dependent pathway and induction of apoptosis, but also autophagy cell death by caspase-dependent pathway. Suggesting there are obvious differences in the different tumor cell death mechanism. Resveratrol induced autophagy Raji cells death may be related to the cathepsin D. 5 resveratrol-induced leukemia cell death role autophagy new findings provide new avenues for the treatment of leukemia. The study found that resveratrol is able to induce apoptosis can be induced autophagy, showing its potential value as a new cancer treatment. The resveratrol treatment leukemia mechanisms differences, their differences with the induction of apoptosis or autophagy pathways related to the different, the resveratrol-induced leukemia cell death pathway is further engaged in apoptosis or autophagy provide reliable experimental material. Moreover, the study confirmed that resveratrol treatment of leukemia through the new death pathway, that is capable of inducing autophagy, provide a theoretical reference for the clinical treatment of tumors of resveratrol. The study findings further support the induction of cell death, there are different ways, through the analysis of the corresponding difference in apoptosis or autophagy death, can provide a new target control of cell death in different diseases, but also for the induction of apoptosis in anti The cancer chemotherapy invalid mechanism study has opened a new method autophagy research. However, the impact of anti-cancer drugs on the role of cell death autophagy also need to be further explored.
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