ABSTRACT
<p><b>AIM</b>To study the effects of ginkgolides (Gin) on the expression of hypoxia-inducible factor-1alpha (H1F-1alpha) in primary cultured cortical neurons treated with CoCl2 and the relationship with ERK signal pathway.</p><p><b>METHODS</b>We observed the effects of Gin (37.5 mg/L) on morphology and viability on primary cultured cortical neurons with treatment of CoCl2 (125 micromol/L). The expression of HIF-1alpha and p-ERK of neurons induced by CoCl2 pretreated with Gin were assessed by Western-blot. We analyzed the relationship between HIF-1alpha expression activated by Gin and ERK signal pathway with treatment of PD98059 (100 micromol/L), a selective inhibitor of ERK.</p><p><b>RESULTS</b>It was shown that Gin had protective effects on CoCl2 damaged neurons by raising the neuronal viability. Some basic expression of HIF-1alpha and p-ERK were observed in normal cultured cortical neurons. The expression of HIF-1alpha and p-ERK increased strikingly when treated with CoCl2 for 4 h. The levels of HIF-1alpha and p-ERK increased even more in the neurons pretreated with Gin for 24 h before CoCl2. The levels of HIF-1alpha and p-ERK were notably inhibited with pretreatment of PD98059, while Gin could prevent this inhibition.</p><p><b>CONCLUSION</b>Gin has protective effects on neurons damaged by CoCl2 which might be related to the increase of the level of HIF-1alpha and the activation of ERK signal pathway.</p>
Subject(s)
Animals , Mice , Cell Hypoxia , Cells, Cultured , Ginkgolides , Pharmacology , Hypoxia-Inducible Factor 1, alpha Subunit , Metabolism , MAP Kinase Signaling System , Mice, Inbred ICR , Neurons , MetabolismABSTRACT
<p><b>AIM</b>To investigate the effect of Safflor yellow on the gene expression of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in neonatal asphyxia.</p><p><b>METHODS</b>30 minutes after SY 7 g/kg weight intraperitoneally was administered on the neonatal rats. After asphyxia for 40 minutes,the neonatal rats were reoxygenated for 48 h, and the nitric oxide synthases (NOSs) mRNA expression was assessed by semi-quantitative reverse transcription-polymerase chain reaction.</p><p><b>RESULTS</b>Neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) were up in hypoxia/reoxygenation (H/R) 48 h group, while both of them were down significantly in SY group, but no change was observed on endothelial nitric oxide synthase (eNOS).</p><p><b>CONCLUSION</b>The protective of SY from brain damage induced by neonatal asphyxia might be associated with expression of NOSs mRNA.</p>
Subject(s)
Animals , Rats , Brain , Metabolism , Chalcone , Pharmacology , Therapeutic Uses , Gene Expression , Hypoxia , Metabolism , Nitric Oxide Synthase Type I , Metabolism , Nitric Oxide Synthase Type II , Metabolism , Nitric Oxide Synthase Type III , Metabolism , Quinones , Pharmacology , Therapeutic Uses , RNA, Messenger , Genetics , Rats, Sprague-DawleyABSTRACT
<p><b>AIM</b>To study the effects of ginkgolides (Gin) on the expression of hypoxia inducible factor-1 (HIF-1alpha) in hypoxic/ischemic neurons.</p><p><b>METHODS</b>The gene expression of HIF-1alpha pretreated with or without Gin (37.5 microg/ml) was observed by RT-PCR on primary cultured cortical neurons in the condition of hypoxia and oxygen-glucose deprivation.</p><p><b>RESULTS</b>Some basic expression of HIF-1alpha mRNA were observed in cultured cortical neurons. The expression of HIF-1alpha mRNA increased after 24 h treatment with Gin. The level of HIF-la mRNA increased also after 1 h hypoxia and further enhanced after the pretreatment with Gin. The expression of HIF-1alpha mRNA decreased with the deprivation of both oxygen and glucose, which reversed after the pretreatment of Gin.</p><p><b>CONCLUSION</b>Gin could increase the expression of HIF-1alpha mRNA in hypoxic/ischemic cortical neurons.</p>