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OBJECTIVE To study the repair effect of ephedrine on lipopolysaccharide （LPS）-induced microglia function injury and its mechanism. METHODS Human microglia cells （HMC3） were used as research objects to investigate the effects of different concentrations of ephedrine （75， 150， 300， 600 μg/mL） on the viability and apoptosis of HMC3 cells. HMC3 cells were divided into control group （without drug intervention）， LPS group （1 μg/mL）， ephedrine group （1 μg/mL LPS+300 μg/mL ephedrine）， BAY11-7082 group [1 μg/mL LPS+5 μmol/L nuclear factor-κB （NF-κB） pathway inhibitor BAY11-7082]， inhibitor group （1 μg/mL LPS+300 μg/mL ephedrine+5 μmol/L BAY11-7082） and activator group （1 μg/mL LPS+300 μg/mL ephedrine+1 μmol/L NF-κB pathway activator Prostratin）. After 24 hours of drug treatment， cell migration， the levels of soluble interleukin-6（sIL-6）， interleukin-10（IL-10）， superoxide dismutase（SOD）and malondialdehyde（MDA）， and the expressions of NF-κB pathway-related proteins were all detected. RESULTS The viability of HMC3 cells could be increased significantly by 300 μg/mL ephedrine， while the apoptotic rate was decreased significantly （P＜0.05）. Compared with the control group， the number of migrating cells was increased significantly in the LPS group； the levels of sIL-6 and MDA， the phosphorylation of NF-κB protein were increased significantly， while the levels of IL-10 and SOD were decreased significantly （P＜0.05）. Compared with the LPS group， the above indexes were reversed significantly in the ephedrine group and BAY11-7082 group （P＜0.05）. Compared with the ephedrine group， the number of migrating cells was decreased significantly in the inhibitor group； the levels of sIL-6 and MDA， the phosphorylation of NF-κB protein were decreased significantly， while the levels of IL-10 and SOD were increased significantly （P＜0.05）. The above indexes were reversed significantly in the activator group （P＜0.05）can repair cell injury by inhibiting LPS induced apoptosis， migration， inflammation and oxidant stress of HMC3 cells， the mechanism of which may be associated with inhibiting the activity of the NF-κB signaling pathway.
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Objective To improve the clinical efficacy of angina pectoris with dyslipidemia patients, analysis of the combined use of trimetazidine, atorvastatin calcium, the clinical value of psychological intervention.Methods 86 cases of patients with coronary heart disease and angina pectoris with dyslipidemia were selected, according to the random number table method is divided into control group and study group, each group of 43 cases. The control group were given routine symptomatic angina pectoris of coronary heart disease with abnormal blood lipid therapy plus trimetazidine hydrochloride oral Sibutramine, study group on the basis of the control group given oral atorvastatin calcium plus psychological intervention of statin treatment. Results After treatment, the clinical efficiency of the study group and the control group was 95.34％ and 81.4％, the difference between the two groups was statistically significant (P<0.05); patients in the study group SDS, SAS score than the control group, the difference between the two groups was statistically significant (P<0.05); patients in the study group, TC, TG, LDL and C levels were significantly lower than the control group, the HDL level of C higher than that of control group, the difference between the two groups was statistically significant (P<0.05); study on patients with angina pectoris attack times less than the control group, the seizure duration shorter than the control group, the difference between the two groups was statistically significant (P<0.05). Conclusion Psychological intervention combined with the treatment of angina pectoris of coronary heart disease with abnormal blood lipid, clinical efficiency increased from 81.4％ to 95.34％, reduced in patients with depression, anxiety and other negative emotions, so that the blood has been effectively controlled, improve clinical symptoms, reduce the pain of patients, with high clinical value.
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<p><b>OBJECTIVES</b>To assess the culture and differentiation of neural stem cells in embryonic mice and set up a basis for further research in to neural stem cells.</p><p><b>METHODS</b>Embryonic cortices of mice were dissociated and single cell suspensions were achieved by mechanical methods in sterile conditions, and cells were seeded in uncoated plate in N2 medium. The cells were passaged by mechanical methods, frozen and thawed by general procedure. They were identified by immunocytochemical techniques.</p><p><b>RESULTS</b>Neural stem cells from embryonic mice were successfully cultured forming typical neurospheres in suspension. Neurons, astrocytes and oligodendrocytes were differentiated from neural stem cells, with a ratio of 7%, 85% - 90% and 2% - 4% respectively.</p><p><b>CONCLUSIONS</b>Neural stem cells, which can be cultured and passaged steadily in vitro and they are the ideal cell sources for cell transplantation and gene therapy.</p>