Glucose-deprivation으로 유발된 PC-12 cell의 세포 고사에 대한 黃連解毒湯의 보호 효과
Neuroprotective Effect of Hwangryunhaedok-tang Against Glucose-deprivation Induced Cytotoxicity in PC-12 Cells
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The purpose of the study was to confirm what effect HRHDT treatment had on cell extinction by damage of endoplasmic reticulum induced to PC-12 cell damage by glucose deprivation. The study confirmed what effect it had on forming the condition of glucose deprivation within a culture fluid of PC-12 cell and on a nerve cell＇s survival rates and tested whether HRHDT could prevent extinction of PC-12 cell by glucose deprivation. Also, the study confirmed what effect HRHDT treatment had on the emitted quantity of LDH by glucose deprivation. To examine PC-12 cell＇s behavioral change under the condition of glucose deprivation and a protective effect of HRHDT on the change, the study observed PC-12 cell＇s behavioral change with a microscope. Also, the study confirmed density of calcium ion within cells followed by a culture time in the condition of glucose deprivation with FACS and confirmed what effect HRHDT treatment had on the above density of calcium ion within cells. Finally, the study carried out the western blot and confirmed what effect HRHDT treatment had on revelation of GRP 78 and CHOP protein and a segmental type of aspase 12. In this study, HRHDT rescued PC-12 cells from glucose deprivation-induced cell death. HRHDT also prevents the LDH release, Ca++ accumulation, and morphological change, which was associated with the ER stress. Furthermore, HRHDT reduced the expression of ER chaperone (Grp78 and CHOP) proteins by glucose deprivation in PC-12 cells. These results suggest that HRHDT might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by glucose deprivation injuries.
Abstract
The purpose of the study was to confirm what effect HRHDT treatment had on cell extinction by damage of endoplasmic reticulum induced to PC-12 cell damage by glucose deprivation. The study confirmed what effect it had on forming the condition of glucose deprivation within a culture fluid of PC-12 cell and on a nerve cell＇s survival rates and tested whether HRHDT could prevent extinction of PC-12 cell by glucose deprivation. Also, the study confirmed what effect HRHDT treatment had on the emitted quantity of LDH by glucose deprivation. To examine PC-12 cell＇s behavioral change under the condition of glucose deprivation and a protective effect of HRHDT on the change, the study observed PC-12 cell＇s behavioral change with a microscope. Also, the study confirmed density of calcium ion within cells followed by a culture time in the condition of glucose deprivation with FACS and confirmed what effect HRHDT treatment had on the above density of calcium ion within cells. Finally, the study carried out the western blot and confirmed what effect HRHDT treatment had on revelation of GRP 78 and CHOP protein and a segmental type of aspase 12. In this study, HRHDT rescued PC-12 cells from glucose deprivation-induced cell death. HRHDT also prevents the LDH release, Ca++ accumulation, and morphological change, which was associated with the ER stress. Furthermore, HRHDT reduced the expression of ER chaperone (Grp78 and CHOP) proteins by glucose deprivation in PC-12 cells. These results suggest that HRHDT might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by glucose deprivation injuries.
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