title: Monosialotetrahexosy-1 ganglioside attenuates diabetes-enhanced brain damage after transient forebrain ischemia and suppresses phosphorylation of ERK1/2 in the rat brain.
abstract: Monosialotetrahexosy-1 ganglioside (GM1) has been shown to reduce brain damage induced by cerebral ischemia. The objective of this study is to determine whether GM1 is able to ameliorate hyperglycemia-exacerbated ischemic brain damage in hyperglycemia-recruited areas such as the hippocampal CA3 sub regions and the cingulated cortex. Histologic stainings of Haematoxylin and Eosin, Nissl body, the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and phospho-ERK1/2 were performed on brain sections that have been subjected to 15 min of forebrain ischemia with reperfusion of 0, 1, 3, and 6h in normoglycemic, hyperglycemic and GM1-pretreated hyperglycemic groups. The results showed that GM1 ameliorated ischemic neuronal injuries in the CA3 area and cingulated cortex of the hyperglycemic animals after ischemia and reperfusion. Immunohistochemistry of phospho-ERK1/2 revealed that the neuroprotective effects of GM1 were associated with suppression of phospho-ERK1/2. The results suggest that GM1 attenuates diabetic-augmented ischemic neuronal injuries probably through suppression of ERK1/2 phosphorylation.
authors.affiliation: Department of Pathology, Ningxia Medical University, Yinchuan 750004, PR China. zhangjz@nxmu.edu.cn
authors.forename: Jian-Zhong
authors.initials: JZ
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Jing
authors.forename: Yi
authors.initials: Y
authors.lastname: Ma
authors.forename: Feng-Ying
authors.initials: FY
authors.lastname: Guo
authors.forename: Yue
authors.initials: Y
authors.lastname: Chang
authors.forename: P Andy
authors.initials: PA
authors.lastname: Li
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications*; D004195:Disease Models, Animal; D005677:G(M1) Ganglioside / Q000627:therapeutic use*; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D002534:Hypoxia, Brain / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D020287:In Situ Nick-End Labeling / Q000379:methods; D008297:Male; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D009410:Nerve Degeneration / Q000188:drug therapy / Q000209:etiology; D009474:Neurons / Q000187:drug effects; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013311:Streptozocin; D013997:Time Factors
chemical_list: D018696:Neuroprotective Agents; D005677:G(M1) Ganglioside; D013311:Streptozocin; D048052:Mitogen-Activated Protein Kinase 3