ABSTRACT
The present paper is aimedto investigate the effect of basic fibroblast growth factor (bFGF) on proliferation, migration and differentiation of endogenous neural stem cell in rat cerebral cortex with global brain ischemia-reperfusion. A global brain ischemia-reperfusion model was established. Immunohistochemistry was used to observe the pathological changes and the expression of BrdU and Nestin in cerebral cortex. RT-PCR was used to measure the NSE mRNA in brain tissue. The results of measurements indicated that in sham operation group, there was no positive cell in cerebral cortex, and the content of NSE mRNA did not change. In the operation group, the expression of BrdU and Nestin increased significantly at the end of the 3rd day, and peaked on the 7th day. NSE mRNA expression did not significantly increase. In bFGF group, compared with sham operation group and model group, the number of BrdU-positive and Nestin-positive cells increased significantly at each time point (P<0. 05), and peaked at the end of the 11th day, and the content of NSE mRNA increased significantly (P<0. 05). This research demonstrated that the proliferation of endogenous neural stem cells in situ could be induced by global cerebral ischemia and reperfu- sion, and could be promoted and extended by bFGF. In additiion, bFGF might promote endogenous neural stem cells differentiated into neurons.
Subject(s)
Animals , Rats , Brain Ischemia , Pathology , Cell Differentiation , Cell Movement , Cell Proliferation , Cerebral Cortex , Cell Biology , Metabolism , Pathology , Fibroblast Growth Factor 2 , Pharmacology , Nestin , Metabolism , Neural Stem Cells , Reperfusion InjuryABSTRACT
To study the effect of the proliferation and apoptosis of Survivin-T34A mutant on breast cancer MCF-7 cell, we adopted the method of cell culture in vitro to observe the proliferation and apoptosis of the cell. In the experiment, MCF-7 cells were randomly divided into three groups and transfected with normal saline, PORF-9-null and Survivin-T34A, respectively. Breast cancer nude mouse models were established to study anti-tumor effect of Survivin-T34A in vivo. The activity of the cells in the Survivin-T34A-transfected group was lower than that in PORF-9-null group. The increase of cell apoptosis was observed under electron microscopy, meanwhile the apoptotic rate was obviously higher than that in PORF-9-null control by flow cytometry. Tumor inhibition effects of the mouse which received the injection of Survivin-T34A intratumoral injection were apparent, and the inhibition ratio was as high as 47.1%. In conclusion, Survivin-T34A mutant has anti-tumor effect through efficiently inhibiting the growth of breast cancer MCF-7 cell and actively promoting apoptosis of cancer cells.
Subject(s)
Animals , Humans , Mice , Apoptosis , Breast Neoplasms , Drug Therapy , Pathology , Inhibitor of Apoptosis Proteins , Genetics , Pharmacology , Injections, Intralesional , Mice, Nude , Neoplasm Transplantation , TransfectionABSTRACT
Objective To explore the influence of icotinib in the apoptosis of the human salivary adenoid cystic carcinoma cells ACC-M, and to clarify the mechanism of icotinib for the treatment of salivary adenoid cystic carcinoma.Methods The ACC-M cells were randomly divided into control group,2,4,8μmo1·L-1 icotinib groups,p38-MAPK inhibitor SB203580 (20μmol· L-1 )group,SB203580 (20 μmol· L-1 )+4μmo1 · L-1 icotinib group;the cells were collected 4 h after treatment.The viability of ACC-M cells was measured by MTT assay.The apoptosis of ACC-M cells was assessed by caspase-3 activity kit. The expression of p-p38-MAPK protein was determined by Western blotting analysis.Results Compared with control group,the inhibitory rates of growth of the ACC-M cells in icotinib groups were significantly decreased (P<0.05 ), and the activities of caspase-3 were increased (P<0.05),and the expression levels of p-p38-MAPK were significantly increased (P<0.05).Compared with 4μmo1·L-1 icotinib group,the expression level of p-p38-MAPK in SB203580+icotinib group were decreased (P < 0.05 ), and the activity of caspase-3 was decreased dramatically (P < 0.05 ). Conclusion Icotinib may induce the apoptosis of ACC-M cells through the activation of p38-MAPK signaling pathway.