Journal of International Academy of Physical Therapy Research (국제물리치료학회지)

International Academy of Physical Therapy Research (국제물리치료연구학회)
권호 표지
DOI QR코드

DOI QR Code

Effects of NEES on PARP Expression in the Corpus Striatum in Rats Induced with Transient Global Ischemia

  • Received : 2012.05.29
  • Accepted : 2012.08.24
  • Published : 2012.10.31
Download PDF
⟨ Previous Next ⟩

Abstract

Ischemia, the leading cause of strokes, is known to be deeply related to synaptic plasticity and apoptosis in tissue damage due to ischemic conditions or trauma. The purpose of this study was to research the effects of NEES(needle electrode electrical stimulation) in brain cells of ischemia-induced rat, more specifically the effects of Poly[ADP-ribose] polymerase(PARP) on the corpus striatum. 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, and at 24 hours post-ischemia on the hapgok. Protein expression was investigated through PARP antibody immuno-reactive cells in the cerebral nerve cells and western blotting. The number of PARP reactive cells in the corpus striatum 24 hours post-ischemia was significantly(p<.05) smaller in the NEES group compared to the global ischemia(GI) group. PARP expression 24 hours post-ischemia was very significantly smaller in the NEES group compared to the GI group. Results show that ischemia increases PARP expression and stimulates necrosis, making it a leading cause of death of nerve cells. NEES can decrease protein expression related to cell death, protecting neurons and preventing neuronal apoptosis.

Keywords

References

  1. Sharp FR, Lu A, Tang Y, Millhorn DE. Multiple molecular penumbras after cerebral ischemia. J Cereb Blood Flow Metab 2000; 20: 1011-1032.
  2. Ikai K, Ueda K, Hayaishi O. Immunohistochemical demonstration of poly(adenosinedephophate- rebose) in nuclei of various rat tissues. J Histochem Cytochem 1998; 28: 670-676.
  3. Ogura T, Takenouchi N, Yamaguchi M, Matsukage A, Sugimura T, Esumi H. Striking similarity of the distribution patterns of the poly(ADP-ribose) polymerase and DNA polymerase beta among various mouse organs. Biochem Biophys Res Commun 1990; 172: 377-384. https://doi.org/10.1016/0006-291X(90)90683-E
  4. Vispe S, Yung TM, Ritchot J, Serizawa H, Satoh MS. A cellular defense pathway regulating transcription through poly(ADP-ribosyl) action in response to DNA damage. Proc Natl Acad Sci USA 2000; 97: 9886-9891. https://doi.org/10.1073/pnas.170280397
  5. Zhang J, Pieper A, Snyder SH. Poly(ADP-ribose) synthetase activation, an early indicator of neurotoxic DNA damage. J Neurochem 1995; 65:1411-1414.
  6. Berger NA. Poly(ADP-ribose) in the cellular response to DNA damage. Radiat Res 1985; 101:14-15.
  7. Schraufstatter IU, Hyslop PA, Hinshaw DB, Spragg RG, Sklar LA and Cochrane CG. Hydrogene peroxideinduced injury of cells and its prevention by inhibitors of poly(ADP-ribose) polymerase. Proc Natl Acad Sci USA 1986; 83:4908-4912. https://doi.org/10.1073/pnas.83.13.4908
  8. Zhang J, Dawson VL, Dawson TM, Snyder SH. Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity Science 1994; 263: 687-689. https://doi.org/10.1126/science.8080500
  9. Virag L, Salzmannnn AL, Szabo C. Poly(ADPribose) synthetase activation mediates mitochondrial injury during oxidant induced cell death. J Immunol 1998; 161: 3753-3759.
  10. Karczewski JM, Peters JG, Noordhoek J. Prevention of oxidant-induced cell death in Caco-2 colon carcinoma cells after inhibition of poly(ADP-ribose) polymerase and Ca2+ chelation, involvement of a common mechanism. Biochem Pharmacol 1999; 57: 19-26. https://doi.org/10.1016/S0006-2952(98)00286-X
  11. Ha HC, Snyder SH. Poly(ADP-ribose) polymerase is a mediator of necrotic cell death by ATP depletion. Proc Natl Acad Sci USA 1999; 96: 13978-13982. https://doi.org/10.1073/pnas.96.24.13978
  12. Wallis RA, Panizzon KL, Henry D, Wasterlain CG. Neuroprotection against nitric oxide injury with inhibitors of ADP-ribosyltion. Neuroreport 1993; 5: 245-248.
  13. Kirino T, Tamura A, Sano K. Delayed neuronal death in the rat hippocampus following transient forebrain ischemia. Acta Neuropathol 1984; 64:139-147. https://doi.org/10.1007/BF00695577
  14. Abe Y, Mishiro K, Takanashi M. Symbiont of brown-winged green bug Plautia stali Scott. Japanese Journal of Applied Entomology and Zoology 1995; 39: 109-115. https://doi.org/10.1303/jjaez.39.109
  15. Kim DK. Immunohistochemical studies on the regulation of enteroendocrine cells of GI tract and neurotransmitters of CNS to electroacupunctures stimulation of Zusanli acupoints(ST36). Woosuk University 2009.
  16. Son SS. Effect of different patterns and stimulation duration of electroacupuncture on the neuronal activities in the spinal using Fos immunohistochemical techniques. Thesis for Degree of Doctor of Oriental Medicine 1985.
  17. Li X, Nemoto M, Xu Z, Yu SW, Shimoji M, Andrabi SA, Haince JF, Poirier GG, Dawson TM, Dawson VL, and Koehler RC. Influence of Duration of Focal Cerebral and neuronal nitiric oxide synthase on translocation of apoptosisinducing factor to the nucleus. Neuroscience 2007; 144: 56-65. https://doi.org/10.1016/j.neuroscience.2006.08.065
  18. Nicoletti VG and Stella AM. Role of PARP under stress conditions; cell death or protection. Neurochemical Res 2003; 28: 187-94. https://doi.org/10.1023/A:1022316914492
  19. Endres M, Wang ZQ, Namura S, Waeber C, Moskowitz MA. Ischemic brain injury is mediated by the activation of poly(ADP-ribose) polymerase. J Cereb Blood Flow Metab 1997; 17: 1143-1151.
  20. Tokime T, Nozaki K, Sugino T, Kikuchi H, Hashimoto N, Ueda K. Enhanced poly(ADPribolsyl) ation after focal ischemia in rat brain. J Cereb Blood Flow Metab 1998; 18: 991-997.
  21. Wallis RA, Panizzon KL, Henry D, Wasterlain CG. Neuroprotection against nitric oxide injury with inhibitors of ADP-ribosyltion. Neuroreport 1993; 5: 245-248.
  22. Cosi C, Suzuki H, Milani D, Facci L, Vantini G, Kanai Y, Skaper SD. Poly(ADP-ribose) polymerase: early involvement in glutamate-induced neurotoxicity in cultured cerebellar granule cells. J Neurosci Res 1994; 39: 38-46. https://doi.org/10.1002/jnr.490390106
  23. Thiemermann C, Bowes J, Myint F, Vane JR. Inhibition of activity of poly(ADP)ribose synthetase reduces ischemia-reperfusion injury in the heart and skeletal muscle. Proc Natl Acad Sci USA 1997; 94: 679-683. https://doi.org/10.1073/pnas.94.2.679
  24. Schraufstatter IU, Hyslop PA, Hinshaw DB, Spragg RG, Sklar, LA, Cochrane CG. Hydrogene peroxideinduced injury of cells and its prevention by inhibitors of poly(ADP-ribose) polymerase. Proc Natl Acad Sci USA 1986; 83: 4908-4912. https://doi.org/10.1073/pnas.83.13.4908
  25. Cuzzocrea S, Zingarelli B, O'Connor M, Salzman AL, Caputi AP, Szabo C, Role of peroxynitrite in the vascular failure induced by zymosan-activated plasma. Br J Pharmacol 1997; 122: 493-503. https://doi.org/10.1038/sj.bjp.0701387