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目的研究norA基因介导的金葡菌对氟喹诺酮类药物的耐药机制。方法PCR法制备DIG-norA基因探针;点杂交及狭线杂交检测细菌norA基因及其转录水平。结果所有实验菌株均检测到norA基因;诱导耐药菌SA2-16的norA基因转录水平明显高于其亲代株,临床分离耐药菌norA基因转录水平略高于敏感菌,但统计学分析无显著性差异,细菌在环丙沙星1/10MIC浓度中生长,未见norA基因转录增加。结论norA基因可能为金葡菌的结构基因,诱导耐药菌药物泵出增加的原因在于norA基因转录的增加,norA基因介导的耐药在不同的耐药菌株中所起的作用并不相同。
Objective To investigate the mechanism of norA gene-mediated S. aureus fluoroquinolones resistance. Methods DIG-norA gene probe was prepared by PCR method. The norA gene and its transcription level were detected by dot blot hybridization and narrow-line hybridization. Results The norA gene was detected in all the experimental strains. The transcription level of norA gene in the resistant strain SA2-16 was significantly higher than that in the parental strain. The transcription level of norA gene in clinical isolates was slightly higher than that in the susceptible strains, but the statistical analysis showed no significant difference The differences in sex, bacteria in ciprofloxacin 1 / 10MIC concentration of growth, no increase in norA gene transcription. CONCLUSIONS: norA gene may be the structural gene of S.aureus. The reason for the increase of the resistance to drug-induced drug pumpout is the increase of transcription of norA gene. The norA gene-mediated resistance plays a different role in different drug-resistant strains .