ABSTRACT
<p><b>OBJECTIVE</b>To study the effect of panax notoginseng saponins (PNS) in treating hemorrhagic apoplexy at super-early stage in rats.</p><p><b>METHODS</b>Rat model of hypertension with cerebral hemorrhage was induced by collagenase method. Sixty rats were randomly divided into 5 groups: the sham operated group, model group, PNS high, middle, and low dose group, 12 in each; 4 h after modeling, PNS or normal saline was intraperitoneally injected into the rats every 12 h, the total is 5 times. Contents of water, sodium and potassium ion in brain, and the diameter of hematoma in rats of different groups were measured 24 h and 72 h after modeling.</p><p><b>RESULTS</b>Compared with the model rats, nerve defect symptoms aggravated, the contents of water and sodium ion in ipsilateral cortex and basal ganglia were significantly higher, the content of potassium ion was lower and the hematoma diameter was obviously less in the PNS-treated rats (all P < 0.05).</p><p><b>CONCLUSION</b>PNS may worsen the brain edema and increase the nerve defect score when it was applied at the early stage of cerebral hemorrhage, but could promote the absorption of hematoma, indicating PNS should be used cautiously in treating patients with large amount of cerebral hemorrhage at super-early stage.</p>
Subject(s)
Animals , Male , Rats , Brain Edema , Drug Therapy , Cerebral Hemorrhage , Injections, Intraperitoneal , Panax notoginseng , Chemistry , Phytotherapy , Random Allocation , Rats, Sprague-Dawley , Saponins , Therapeutic Uses , Time FactorsABSTRACT
@#ObjectiveTo explore the effects of the serum of traditional Chinese medicine Nao Yi An on glutamate induced cell death in cultured hippocampal neurons of rat and the underlying mechanisms. MethodsHippocampal neurons were cultured. The excitatory amino acid induced toxicity on cultured neurons was investigated. The viability of injured neurons was determined with the measurement of Lactate dehydrogenase (LDH) activity. Mitogen activated protein kinase (MAPK) were determined by immunoprecipitation /kinase assays /western blot detection.ResultsThe serum of Nao Yi-An raised cell viability. The serum of Nao Yi-An upregulated the expression of extracellular regulated protein kinases(ERK) and downregulated the expression of c-Jun N terminal kinase/stress activited protein kinase(JNK) in cultured neurons. The serum of Nao Yi-An induced upregulation of ERK and its anti death action were prevented with the specific ERKs inhibitor PD98059. Conclusions Activation of ERK signaling together with inhibition of JNK signaling by Chinese medicine Nao Yi-An appears to be an important mechanism for its survival effects on cultured hippocampal neurons.