Sodium thurasilin is a compound antibiotic formulation, of which thalasilin is a semi-synthetic penicillin-like antibiotic, and thurathan is a beta-neamide inhibitor. Their joint use can effectively combat multiple bacterial infections.
1. Interference in the synthesis of bacterial cytowalls The main component of the cell wall is aluminum, and its synthesis is a complex process. There are many enzymes involved in the process of condensation, and penicillin combined proteins (PBPs) play a key regulatory role. • The chemical structure of Zolasilin contains the beta-nimide ring, which is the core of its antibacterial activity. When Zolasilin enters the environment surrounding the bacteria, it is able to combine with the PBPs on the bacterial membranes. The combination is highly specific, as if a key had been inserted into the corresponding lock. • The normal functioning of the PBPs is inhibited by the combination of Zolasilin and PBPs. When the PBPs function is blocked, key steps, such as the conjunctive reaction in the process of plaster synthesis, cannot proceed normally. For example, in the gelatin cactus, albeit thin, the glycol layer remains an important part of the cell wall, which may be disrupted by the Zolacillin process and its integrity damaged. In the gland positive bacteria, due to the thickness of the cytal glucose layer, the role of Zaracillin is more visible and can more effectively destroy the cell wall structure. • As cell wall synthesis is blocked, bacteria lose effective protection of cell wall. Because the internal pressure of bacteria is higher than in the outside environment, bacteria can swell as a result of water inhalation in the absence of a complete cell wall. Ultimately, bacteria die as a result of cell walls that cannot withstand internal pressure. 2. Antibacterial spectra — Zaracillin has a high level of antibacterial activity in a variety of gelatines, such as coli-Eshi, Creber, and copper-coloured singles. It’s because it can penetrate the outer membranes of the gelatin fungus, and it’s working in the glycol synthesis. At the same time, it has some anti-bacterial effects on some of the gland positive bacteria, although relatively weak.
1. The inhibition of beta-nimamine enzyme — bacterium produced beta-nimide enzyme in order to resist the effects of beta-implamide antibiotics. This enzyme hydrolyzes the beta-nimide antibiotic β-imperamide rings, which deprives them of antibacterial activity. For example, bacteria that are resistant to drugs, such as those that produce ultra-spectrum β-ESBLs, can damage antibiotics by creating them. • Shubathan is an irreversible and competitive beta-nimide inhibitor. It has a chemical structure similar to that of β-NEA, which can be combined with β-NEA. When combined with the active part of the β-nimide enzyme, it prevents the hydrolysis of the enzyme to the Zolasilin, thus protecting the β-nimide ring from destruction. • This protective effect enables the Zolacillin to continue its antibacterial activity and effectively suppresses the synthesis of bacterial cell walls. When used jointly by Shubatan and Zolasicillin, there is a synergistic antibacterial effect that can expand the antibacterial spectrum and enhance the antibacterial effect on drug-resistant bacteria.
When sodium sodium sodium sambatane enters the human body, schubathan will be the first to act as a inhibitor of β-neamidease and to create a good antibacterial environment for Zolacillin. The Zolasilin can then successfully combine with the PBPs on the bacterial membranes, interfering with the synthesis of bacterial cell walls. This joint mechanism enables the compound to effectively treat infections caused by a variety of drug-resistant bacteria, such as hospital access to pneumonia, complex abdominal infections, and urinary system infections. In the course of treatment, they work together, increasing the lethality of bacteria and the success rate of treatment.
