After testing the resistance of streptomycin to NS-41-80 Streptomyces Nanchangensis NS-41-80, the spores treated with 4 different dosage of super-mutagent EMS were regenerated on the lethal media, thus 3,000 streptomycin-resistant ( str ) str mutants were obtained. Then 202 spore mutants were screened through the pre-screening experiments and their yields are beyond 20% higher than the original strains respectively. In the re-screening experiments 48, 7 and 1 mutants were obtained whose yields are 100%, 200% and 300% higher than the original strains respectively and take the precentage of 23.76% and 1.60%, 3.46% and 0.23% and 0.5% and 0.03% of the number of the pre-screened strains and the rescreened strains respectively. Then 5 mutants were fermented whose yields are above 240% higher and the original strain through the continuous 3 batches fermentation, the yields are 57%～96.4% more than the original strains. Among them the yield of 80-5.3-165 is upwards of 6,000?g/mL and its norm is 5,855?g/mL. And a model of the streptomycin-resistance mutational screening of the strain producing Nanchangmycin was established.

OBJECTIVE: To observe the protective effect of Huaxia shallot preparation on human umbilical vein endothelial cell (HUVEC) injury induced by oxidized low density lipoprotein (Ox-LDL) in vitro. METHODS: Ox-LDL was prepared and identified, and HUVECs were cultured. After 2-hour intervention of different drugs and 24-hour following intervention of Ox-LDL, the number of HUVECs was observed by phase contrast optical microscope and the activity of the HUVECs was observed by methyl thiazolyl tetrazolium (MTT) technique. Superoxide dismutase (SOD) activity and nitric oxide (NO) content were assayed by respective kit. The protein expressions and mRNA levels of peroxisome proliferators activated receptor gamma(PPAR-gamma) and endothelial nitric oxide synthase (eNOS) were measured by western blot technique and reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Ox-LDL could increase the apoptosis rate of the HUVECs and decrease the NO release as compared with the blank control group (P<0.05). These effects induced by Ox-LDL were all significantly inhibited by Huaxia shallot preparation. It could up-regulate the protein expressions and mRNA levels of PPAR-gamma and eNOS significantly (P<0.05). Huaxia shallot preparation could decrease the apoptosis rate of the HUVECs. CONCLUSION: Ox-LDL may be involved in the initiation and progression of atherosclerosis by injuring the endothelial cells directly and may cause the endothelial dysfunction. Huaxia shallot preparation can protect against Ox-LDL induced endothelial cell injury by up-regulating the protein expressions and mRNA levels of PPAR-gamma and eNOS. It suggests that Huaxia shallot preparation may play a role in the prevention and treatment of cardiovascular disease.