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This study aimed to develop a cell culture model of Huntington disease and observe the effect of sodium butyrate on this cell culture model.Exon 1 of both a wild type and a mutant IT15 gene from the genomic DNA of a healthy adult and a patient with Hunt- ington disease was amplified and cloned into the eukaryotic expression vector pEGFP-C1.Human neuroblastoma SH-SY5Y cells were tran- siently transfected with these recombinant plasmids in the absence and presence of sodium butyrate(0.1,0.2,0.5,1.0 mmol/L).The MTT assay was used to measure cell viability.The results indicated that the N-terminal fragment of mutant huntingtin formed perinuclear and intranuclear aggregates and caused a decrease of SH-SY5Y cell viability.Sodium butyrate inhibited the decrease of SH-SY5Y cell via- bility caused by the N-terminal fragment of mutant huntingtin.This suggests that sodium butyrate has a protective effect on this cell cul- ture model of Huntington disease.
This study aimed to develop a cell culture model of Huntington disease and observe the effect of sodium butyrate on this cell culture model. Exon 1 of both a wild type and a mutant IT15 gene from the genomic DNA of a healthy adult and a patient with Hunt - ington disease was amplified and cloned into the eukaryotic expression vector pEGFP-C1. Human neuroblastoma SH-SY5Y cells were tran-siently transfected with these recombinant plasmids in the absence and presence of sodium butyrate (0.1, 0.2, 0.5, 1.0 mmol / L ). The MTT assay was used to measure cell viability. The results indicated that the N-terminal fragment of mutant huntingtin formed perinuclear and intranuclear aggregates and caused a decrease in SH-SY5Y cell viability. Sodium butyrate inhibited the decrease of SH-SY5Y cell via-bility caused by the N-terminal fragment of mutant huntingtin. This suggests that sodium butyrate has a protective effect on this cell culture model of Huntington disease.