Brain cell death mechanism induced by high-dose dexamethasone
BAO Cui-Fen, YUAN Jing, LIANG Jia, DIAO Rong
Chinese Journal of Clinical Anatomy ›› 2013, Vol. 31 ›› Issue (2) : 184-187.
Brain cell death mechanism induced by high-dose dexamethasone
Objective To investigate the brain cell death mechanism induced by high-dose dexamethasone. Methods SD rats were randomly divided into the control group and the experimental group. The experimental group was divided into 7d, 9d, 11d three subgroups. The experimental group received intraperitoneal injection of DX 5mg/kg while the control group received injection with equal volume of physiological saline. light microscopy, electron microscopy, immunohistochemistry and western blot were used to observe the morphological changes of the brain tissue and detect the expression of Active Caspase-3, PARP-1, pULK1 of the brain tissue. Results (1) rat brain tissue structure was clear and normal in the control group. In the 7d experimental group, the brain tissue had no significant pathological changes. Apoptosis and oncosis of the brain cells were observed in the 11d experimental group. (2) In the control group, expression of active Caspase-3, PARP-1, pULK1 was negative. Compared with the control group, expression levels of active Caspase-3, PARP-1,pULK1 were gradually increased with the treatment time in the brain tissue of the experimental group. Conclusion Brain cell death in dexamethasone-induced may be through the activation of Caspase-3 ,PARP-1, pULK1.
Dexamethasone / Brain cells / Caspase3 / (ADP-ribose) polymerase / Phospho-ULK1
[1] Baum P, Bercker S, Villmann T, et al.Critical illness myopathy and neuropathy (CRIMYN). Electroneurographic classification
[J]. Nervenarzt, 2011,82(4):468-474.
[2] Hermans G, De Jonghe B, Bruyninckx F, et al. Clinical review: Critical illness polyneuropathy and myopathy
[J].Crit Care，2008,12(6):238.
[3] Stevens RD, Hart N, de Jonghe B, et al. Weakness in the ICU: a call to action
[J]. Crit Care, 2009,13(6):1002.
[4] Mozaffar T, Haddad F, Zeng M, et al. Molecular and cellular defects of skeletal muscle in an animal model of acute quadriplegic myopathy
[J]. Muscle Nerve, 2007, 35(1):55-65.
[5] Chu X, Fu X, Zou L, et al. Oncosis, the possible cell death pathway in astrocytes after focal cerebral ischemia
[J]. Brain Res, 2007,29(1149):157-164.
[6] Wyllie AH. Apoptosis: cell death in tissue regulation
[J]. J Pathol,1987,153(4): 313-316.
[7] Kroemer G, El-Deiry WS, Golstein P, et al. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death
[J]. Cell Death Differ，2005，12（suppl 2）：1463-1467.
[8] Shimizu S. Apoptosis and non-apoptotic cell death
[J]. Rinsho Ketsueki,2011, 52(10): 1669-1676.
[9] Wilson MR. Apoptosis: unmasking the executioner
[J].Cell Death Differ,1998,5(8):646-652.
[10] Andrabi SA, Dawson TM, Dawson VL. Mitochondrial and nuclear cross talk in cell death: parthanatos
[J]. Ann N Y Acad Sci, 2008,1147:233-241.
[11]Cheong H, Lindsten T, Wu J, et al. Ammonia-induced autophagy is independent of ULK1/ULK2 kinases
[J].Proc Natl Acad Sci USA, 2011,108(27):11121-11126.
[12] Lee EJ, Tournier C. The requirement of uncoordinated 51-like kinase 1 (ULK1) and ULK2 in the regulation of autophagy
[J].Autophagy,2011,7(7):689-695.
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