Vancocin is an antibiotic of aluminum and is used mainly for the treatment of serious infections caused by the Geran positive. Its mechanisms are as follows:
1. Combining with the bacterium-cellular glucose precursor • The bacterium-cell wall plays a key role in the survival and maintenance of normal patterns of bacteria. Monument is the main component of the bacterium cell wall, and it is a web structure formed by the interlinking of the polymal chain and beryllium. During the synthesis of bacterial cell walls, pelican precursors are produced. • Vancocin is uniquely identified and integrated at the end of the D-propamide-D-Ala-D-Ala. This combination has a high degree of probity, which is a key initial step in the antibacterial role of the vancocin. It’s like a precise key that matches this particular structure in the synthesis of bacterial cell walls.
ii. The inhibition of cell wall synthesis • When vancomicin is combined at the end of the D-Ala-D-Ala precursor, it impedes the use of trans-gluent and trans-gallenes in the process of bacterial cell wall synthesis. The glucose-based effect is to connect the polyglucose chain to the basic skeleton of the cell wall, while the gill function is to connect the beryllium side chain and to increase the strength of the cell wall. • Specifically, the vacocin has prevented normal contact between enzymes involved in cell wall synthesis and aluminum-polymeric precursors through space-level resistance. It inhibits, for example, the activity of transcipher enzymes in the process of polymalization. Transpolytic enzymes are enzymes that act as catalysts for the interlinking of beryllium, which, when combined with vancocin, are not working properly, the conjunctive process of cytex is disrupted and cell wall synthesis is not normal. • This is as if during the construction of a house, vancomicin prevented construction workers (enzymes) from using key building materials (precursors for polymal sugar) and led to a breakdown in the construction of a house (cell walls).
iii. Damage to the integrity of the bacterial membrane • Due to the obstruction of cell wall synthesis, bacteria can cause cell wall defects in order to maintain internal osmosis balance. In such cases, the bacterial membrane is subject to greater pressure. • Over time, the integrity of the bacterial membrane can be compromised. This is because the defects in the cell wall make the membrane more vulnerable to external factors such as changes in osmosis pressure, physical damage, etc. When the membrane integrity is destroyed, the matter inside the bacteria leaks, like a bag full of stuff that breaks through a hole, and the things inside it (e.g. ion, protein, etc.) gradually disappear. • At the same time, external harmful substances are also more readily accessible to bacteria, further disrupting the normal physiological functioning of bacteria and, ultimately, causing bacterial deaths.
iv. Activation mechanisms for drug-resistant bacteria Vancocin remains valid for this drug-resistant fungus. • In the case of MRSA, the resistance mechanism is mainly bacteria that produce a special penicillin-combinant protein (PBP), which prevents the normal integration of β-neamide antibiotics. However, the action target of vancocin is not PBP, and it is still able to inhibit the cell wall synthesis of MRSA through the above-mentioned combination with aluminum-polymeric precursors, thus providing antibacterial resistance to this resistance. • In addition, the mechanisms for the operation of the vancocin make it an important part of the treatment of other drug-resistant Qana positive infections, such as intestinal fungi. The intestinal fungus is resistant to a variety of antibiotics, but it can interfere with the cell wall synthesis process and effectively inhibit the growth and reproduction of intestinal fungus. Vancocin plays a powerful antibacterial role by interfering with the synthesis of bacterial cell walls and undermining the integrity of the cellular membranes, and has an irreplaceable and important position in the treatment of the Grean positive bacterial infections, in particular drug-resistant infections.
