| The intracerebral hemorrhage (ICH) is one of the main subtypes of stroke. It' s a very dangerous disease with high incidence and death rate, also many sequelae. In this paper, we used an animal model of ICH which collagenase was injected into the right caudate patumen (CPu) of rats, to study the injury and repair mechanisms in neurons of the forebrain after intracerebral hemorrhage and the effect of Panax notoginseng saponins. The main experimental techniques we used included HE stain, Nissl' s stain, immunohistochemistry, and In situ hybridization (ISH).1 The expression of the apoptosis regulated genes cysteinyl aspartate specific protease-3 (Caspase-3) and B-cell lymphone/leukemia-2 (Bcl-2) in the rat forebrain after ICH and the effects of Panax notoginseng saponins.Using ISH and immunohistochemical techniques, We found the apoptosis-promoter gene Caspase-3 and Caspase-3p20 expressed principally surrounding hematoma, in layer H-V of the cortex and CA2-CA3 subregions of hippocampus after ICH. The positive cells included neurons and astrocytes, the quantity and the color of the positive cells in the treatment group decreased remarkably. Panax notoginseng saponins could inhibit the transcription of Caspase-3mRNA and the activation of Caspase-3, rescue apoptotic neurons. Bcl-2mRNA and Bcl-2 protein expressed principally surrounding hematoma, frontal cortex, parietal cortex, periform cortex and CArCA4 subregions of hippocampus. The positive cells were mainly neurons. The quantity and the color of the positive cells in the treatment group increased remarkably as compared with control group. Panax notoginseng saponins could inhibit the transcription of Caspase-3mRNA and the activation of Caspase-3 protein, promote the transcription of Bcl-2mRNA and the expression of Bcl-2 protein, rescue apoptotic neurons and support their survival.2 The expression of NGK BDNF* TrkB and P7a?in the rat forebrain after ICH and the effects of Panax notoginseng saponinsThe expression of NGF> BDNF, TrkB decreased in hematoma area after ICH. The expression of NGF, BDNF increased surrounding hematoma, in the cortex and hippocampus. The expression of TrkB increased in the cortex and hippocampus, but the numbers of TrkB positive cells were not high. Panax notoginseng saponins could boost up the express ion of NGF, BDNF, TrkB, especially inCA2, CA3 subfields of hippocampus. NGF, BDNF, TrkB expressed higher in 1 - 3 d after ICH in neurons , after 7d decreased , but remained high level inglial cells. The low affinity receptor p75*1* positive cells increased surrounding hematoma and in cortex after ICH; few were found in hippocampus. Panax notoginseng saponins could reduce its expression. Panax notoginseng saponins could exert the protective and therapeutic effects through both promoting the levelsof NGF, BDNF, TrkB and reducing the level of p751?3 The expression of excitatory amino acids (EAAs) receptors, including NRU NR2Ax NR2B subunits of NMDA receptor and GluR2 subunit of AMPA receptor in the rat forebrain after ICH and the effects of Panax notoginseng saponinsThe expressing levels of NRK M2A, NR2B subunits of NMDA receptor increased respectively surrounding hematoma, in cortex, and hippocampus after ICH, but only a few positive cells were found in hematoma area. The positive cells were mainly neurons. The expressing level of NR1 was much higher than NR2A and NR2B. The overexpression of NMDA receptor was one of the main mechanisms of neuron injury. Panax notoginseng saponins could reduce the express ion of NR1-. NR2A^ NR2B obvious ly, rescue the damaged neurons. GluR2 is a subunit of AMPA receptor. There were not GluR2 positive cells to be found in hematoma area and hippocampus after ICH, but the expression surrounding hematoma and in ipsilateral cortex increased. We suggested that Secondary Injury or mild insults could stimulate the expression of GluR2 in neurons, reduce the permeability of Ca2*, but intense insults or lethal injury induce downregulation of GluR2 and increase AMPA receptor-mediated Ca2* Influx. Panax...
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