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Objective To investigate the effect of early rehabilitation treatment in the patients with small cerebral hemorrhage and its possible mechanisms .Methods 133 patients with cerebral hemorrhage were randomly divided into the routine treatment , non-early rehabilitation and early rehabilitation groups and given the routine drug treatment .The early rehabilitation group and the non-early rehabilitation group were additionally given the rehabilitative training after 2 d and 14 d respectively .The scores of Fugl-Meyer reassessment and the Barthel index were assessed before training and after 4-week training ,and the serum levels of circulat-ing endotheial progenitor cells(EPCs) and vascular endotheial cell growth factors(VEGF) were detected .Results Compared with the routine treatment group and the non-early rehabilitation group ,the scores of Fugl-Meyer reassessment and the Barthel index af-ter treatment in the early rehabilitation group were significantly increased (P< 0 .01) .The serum levels of circulating EPCs and VEGF in the early rehabilitation group were also significantly increased compared with the routine treatment group control (P<0 .01) .Conclusion Early rehabilitation treatment can obviously improve the limb movement function and the daily living ability in the patients with small cerebral hemorrhage ,its mechanisms may be involved with the increase of circulating EPCs and VEGF .
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Objective: This study investigates the biological effects and explores the molecular mechanisms of epigallocate-chin-3-gallate (EGCG) on the apoptosis of the human gastric cancer MGC-803 cells. Methods: After treatment with EGCG, cell apopto-sis was verified by flow cytometry with Annexin V and propidium iodide staining, DNA agarose gel electrophoresis, and transmission electron microscopy. The expression profiles of the apoptosis-related genes in the MGC-803 cells with or without treatment by EGCG for 12 h (100 μmol/L), was identified using SuperArray Human Apoptosis Gene Array. The upregulated Fas-L gene and down-regulated Bag-1 gene were confirmed by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Results: When the MGC-803 cells were treated with EGCG at 25, 50, 100, and 200 μmol/L for 24 h, evident sub-diploid peaks were observed. Under treat-ment with 100 μmol/L for 4, 8, 12, and 24 h, the number of early apoptotic cells was greatly increased. When the cells were treated with 100 μmol/L for 24 h, the DNA extracted from the cells displayed a characteristic ladder pattern with agarose gel electrophoresis. Typi-cal morphological changes were observed by electron microscopy, including cell shrinkage, karyo-pyknosis, and the formation of apop-totic bodies. The differential expressions of eight apoptosis-associated genes were determined by gene array detection. The results of Fas-L and Bag-1 selected for RT-PCR and Western blot were consistent with those of gene array. Conclusion: EGCG induces apoptosis in MGC-803 cells, which might be mediated by a number of specific genes and various signal transduction pathways.
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Background and purpose:To investigate the induction of apoptosis by epigallocatechin-3-gallate(EGCG) in xenograft nude mice with human gastric cancer cells and its molecular mechanism. Methods:Human gastric cancer cells were planted into nude mice in order to establish the cancer model, the different dosages of EGCG were injected intraperitoneally in the nude mice. After treatment, flow cytometry (FCM) was used to detect the apoptosis of implanted tumor cells. Immunohistochemical staining was used to detect the expression of apoptosis-related genes like Bal-2 and Bax in implanted tumor.Results:EGCG significantly inhibited tumor growth after being injecting intraperitoneally in the nude mice. The apoptotic cells in implanted tumor could be detected by flow cytometry with PI staining. The expressions of Bax、Caspase-3 were upregulated and Bcl-2 expression was downregulated in implanted tumor.Conclusions:EGCG could significantly inhibit tumor growth in xenograft nude mice with human gastric cancer cells through inducing apoptosis. The down-regulation of Bcl-2 expression and up-regulation of Bax expression observed could result in the activation of Caspase-3, the pathway might account for the induction of apoptosis.
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Background and purpose:Anticancer mechanism of epigallocatechin-3-gallate(EGCG)remains unclear.This study investigated the role of reactive oxygen species(ROS)in epigallocatechin-3-gallate(EGCG)-induced apoptosis in human gastric cancer MGC803 cells.Methods:The inhibition of MGC803 cells growth was measured by MTT assay.Apoptosis of MGC803 cells was studied by using the AO/EB fluorescence stain.Flow cytometry was used to detect the intracellular ROS level and the rate of apoptosis.Results:EGCG could induce apoptosis of MGC803 cells and increased in the intracellular ROS level.However,after treatment with N-acetyl-L-cystein and an athiol-containing antioxidant,the inhibitory effect of EGCG on MGC803 cells was significantly weakened.The apoptotic rate of the cells and the activity of the intracellular ROS level also decreased dramatically.Conclusion:EGCG can induce apoptosis of MGC803 cells.In turn,the ROS inhibitor can significantly inhibit the apoptosis induced by EGCG in MGC803 cells.These results suggest that the cellular generation of ROS plays a role in initiating EGCG-mediated apoptosis of MGC803 cells.