RESUMO
Mammalian target of rapamycin( mTOR) is a key reg-ulator of aging and aging-related diseases. Rapamycin ( RAPA) induces and promotes the process of cell autophagy through in-hibiting mTOR pathway. Autophagy exerts a crucial role in main-taining the cellular meostasis, which provides essential materials for cell reconstruction, regeneration and repair via degradating the redundant, damaged, or senescent proteins and organelles. Hutchinson Gilford progeria syndrome ( HGPS ) patients are al-ways accompanied with abnormally accumulated progerin in cells. Similar to HGPS, abnormal protein accumulation is the common pathological feature of neurodegenerative diseases, in-cluding Huntington′s disease, Parkinson′s disease, Alzheimer′s disease and so on. Degradation of these abnormal proteins pre-dominantly depends on cell autophagy. Thus, rapamycin is a po-tential anti-aging drug for HGPS and aging-related diseases thera-py. This view focuses on the effects of rapamycin on cell autoph-agy and clinical application in HGPS and neurodegenerative dis-eases.
RESUMO
Objective:To study the biological effects of TCR to hepatoma cell by transfection V?7 to lymphocytes. Methods:TCRV?7 gene was amplified by RT PCR and cloned to expression vector pLXSN. The recombinant was transferred into lymphocytes by Lipfectin Reagent transfection,then the lymphocytes were co cultured with hepatoma cells.The phenotype of lymphocytes was detected on the Flow Cytometry and the ultrastructure of the hepatoma cells was showed by electronic microscope.Results:The lymphocyte amount with TCRV?7 expressing in those being transfected was much more than those no transfection.Apoptosis appeared in the hepatoma cells.Conclusion:TCRV?7 subfamily can recognize hepatoma antigen and stimulate T cell.
RESUMO
Objective:To study the expression of TCRV? subfamily which specially recognize the hepatoma cell antigen and the apoptosis of hepatoma cell induced by McAb costimulated PBLs.Methods:The change of the phenotype of PBLs was studied by flow cell cytometry and the level of the expression of TCRV? was studied by RT-PCR and Southern blot,the PTK by western blot.The hypermicroscopic ultrastructure was observed through transmission electron microscope.Results:The level of CD3 and CD8 of PBLs was significantly increased after acted with hepatoma cells,while there was no change in CD4.The expression of TCRV?7 of PBLs was dramaticly increased and peaked at 4 days.PTK increased correspondently,to 58% compared with 11% in control.Besides anti-CD3 McAb induced lymphocyte apoptosis,the mediated apoptosis of hepatoma cells was found in the other three groups.Conclusion:TCRV?7 was the tumor antigen specific T cell receptor,and it activate the PTK signal pathway.The McAb activated lymphocytes initiated apoptosis in hepatoma cells.