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The Effect that the Application of Time-Based Electrolysis Has on Acute Ischemia

  • Received : 2015.06.08
  • Accepted : 2015.08.02
  • Published : 2015.10.30

Abstract

This neurological damage accelerates the infection reaction of cells and apoptosis at the time of reperfusion after ischemia occurs. BCL-2/BCL-2 allogeneic begeminum has a function of suppressing the apoptosis of cells, and thus it is inferred that the susceptibility of cells to apoptosis is determined by the amount of allogeneic begeminum present which is determined based on the amount of BAX. Ischemia was induced in SD mice by occluding the common carotid artery for 5 minutes, after which blood was re-perfused. NEES was applied to acupuncture points, at 12, 24, and 48 hours post-ischemia on the joksamri, Hapgok. Protein expression was investigated through BAX antibody immuno-reactive cells in the cerebral nerve cells and Western blotting. The results were as follows: In the present study as well, as a result of observation of the change in the number of the BAX reaction cells after the inducement of GI, there was the aspect of most of the BAX reaction cells being observed in the corpus striatum area of the GI group 24 hours after the inducement of ischemia. This revealed the same results as those of previous studies in which the change in the number of BAX reaction cells occurred in all areas while ischemia was in progress. The change in the expression of BAX protein after 24 hours showed that there was a very significant reduction in the NEES group compared to the GI group (p<.01). As a result, a greatest amount of change in the number of BAX immunoreactive cells related to apoptosis 24 hours after ischemia appeared in the NEES group. This study that ischemia increases the expression of BAX that induces apoptosis. Thus, it is determined that ischemia is the main cause of the apoptosis of neurons, and this study reveals that low frequency needle electrode electrical stimulation has the effect of blocking the apoptosis of neurons by reducing protein related to the apoptosis of cells that has increased after ischemia has occurred.

Keywords

References

  1. Du C, Hu R, Csernansky CA, Hsu CY and Choi DW. Very delayed infarction after mild focal cerebral ischemia a role for apoptosis. J Cereb Blood Flow Metab 1996; 16: 195-201. https://doi.org/10.1097/00004647-199603000-00003
  2. Oltvai ZN, Milliman CL, Korsmeyer SJ. BCL-2 heterodimerizes in vivo with a conserved homolog, BAX, that accelerates programmed cell death. Cell 1993; 74: 609-619. https://doi.org/10.1016/0092-8674(93)90509-O
  3. Zheng Z, Zhao H, Steinberg GK, Yenari MA. Cellular and molecular events underlying ischemia-induced neuronal apoptosis. Drug News Perspect 2003; 16: 497-503. https://doi.org/10.1358/dnp.2003.16.8.829348
  4. Hara AT, Iwai and Niwa M. Immunohistoc hemical detection of BAX and Bcl-2 proteins in gerbil hppocampus followiong transient forebrain ischemia. Brain Res 1996; 711: 249-253. https://doi.org/10.1016/0006-8993(95)01436-5
  5. Gibson ME, Han BH, Choi J, Knudson CM, Korsmeyer SJ, Parsadanian M, Holtzman DM. BAX contributes to apoptotic-like death following meonatal hypoxia-ischemia evidence for distinct apoptosis pathways. Mol Med 2001; 7(9): 644-655.
  6. Herdegen T, Kovary, Buhl A, Basal expressionof the inducible transcription factors c-Jun, Jun-B, Jun D, c-Fos, Fos B and Knox-24 in the adult rat brain. J Comp Neurol 1995; 354: 39-59. https://doi.org/10.1002/cne.903540105
  7. Gillardon F, Lenz C, Waschke KF, Krajewski S, Reed JC, Zimmermann M, Kuschinsky W. Altered expression of Bcl-2, Bcl-X, Bax, and c-Fos colocalizes with DNA fragmentation and ischemic cell damage following middle cerebral artery occlusion in rats. Mol Brain Res 1996; 40: 254-260. https://doi.org/10.1016/0169-328X(96)00059-9
  8. Chae CH, The effect of DL-a-lipoic acid supplementation and exercise on bax, bcl-2 mRNA expression and caspase-3 activity in D-galactose induced aging. Graduate school of Sung Kyun Kwan University 2005.
  9. Oltvai ZN, Milliman CL, Korsmeyer SJ, Bcl-2 heterodimerizes in vivo with a conserved homolog bax that accelerates programmed cell death. Cell 1993; 74: 609-619. https://doi.org/10.1016/0092-8674(93)90509-O
  10. Kluck RM, Bossy-Wetzel E, Green DR. The release of cytochrome c from mitochondria; a primary site for Bcl-2 regulation of apoposis. Science 1997; 275: 1132-1136. https://doi.org/10.1126/science.275.5303.1132
  11. Kharbanda S, Pandey P, Sshofield L. Role for Bcl-xL as an inhibitor of cytosolic cytochrome C accumulation in DNA damageinduced apoptosism. Proc Natl Acad Sci USA 1997; 94: 6939-6942. https://doi.org/10.1073/pnas.94.13.6939
  12. Gibson ME, Han BH, Choi J, Knudson CM, Korsmeyer SJ, Parasdanian M, Hotzman DM. Bax contributes to apoptotic-like death following neonatal hypoxia-ischemia, evidence for distinct apoptosis pathways. Mol Med 2001; 7(9): 644-655.
  13. Kim SW. An Effect of Needle Electrode Electrical Stimulation on Inhibition of Neuronal Cell death after Inducing Global Ischemia in the Rat Brain. Graduate school of Dong Eui University 2008.
  14. Lee YS, Park SH, Yun BW, Noh JK. The Effect of Duration of Ischemia and Body Temperature on the Expression of Bax/Bcl-2 in Transient Global Ischemia. Journal of Clinical Neurology 2000; 18(4): 431-438.