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β-内酰胺抗生素对革兰阴性菌的杀菌作用,必须是它能通过外膜,进入周质,抵抗住周质中的β-内酰胺酶的水解或生物失活,使有足够量的游离药物作用于细胞内膜上的靶位PBPs,从而干扰细菌胞壁合成,影响细菌繁殖。其中周质中的β-内酰胺酶是使β-内酰胺抗生素灭活,细菌产生耐药的重要原因。为此国际上许多学者对β-内酰胺酶与β-内酰胺抗生素相互作用进行了深入广泛的研究,并研制出一批对β-内酰胺酶稳定的新一代β-内酰胺抗生素。但是随着新抗生素的大量应用,由β-内酰胺酶介导的耐药菌株仍不断出现,而且当某些药物联用于某些菌株时,由于β-内酰胺酶诱导产生,不仅未出现协同或相加,反而出现相互拮抗。因此,为了防止这种由β-内酰胺酶介导的耐药和药物相互作用,有必要对β-内酰胺酶的产生过程及其影响因素进行探讨,这对临床合理用药和新药的开发具有重要意义。
The bactericidal effect of the β-lactam antibiotic on Gram-negative bacteria must be that it can enter the periplasm through the adventitia, resist the hydrolysis or biological inactivation of β-lactamase in the periplasm, and allow a sufficient amount of free drug action Target cells in the cell membrane PBPs, thereby interfering with bacterial cell wall synthesis, affecting bacterial growth. One of the periplasmic β-lactamase is β-lactam antibiotics inactivated, bacterial resistance to produce an important reason. To this end, many scholars in the world of β-lactamase and β-lactam antibiotics have conducted an extensive and extensive study of the interaction and developed a number of β-lactamase stable new generation β-lactam antibiotics. However, with the extensive use of new antibiotics, β-lactamase-resistant drug-resistant strains continue to emerge, and when certain drugs are used in combination with certain strains, not only do they not occur due to β-lactamase induction Synergistic or additive, but appear antagonistic. Therefore, in order to prevent such β-lactamase-mediated drug resistance and drug interactions, it is necessary to investigate the production process of β-lactamase and its influencing factors, which have clinical utility and new drug development Significance.