The innovative team led by researcher Wang Jianhua from the Feed Research Institute of the Chinese Academy of Agricultural Sciences has successfully created an antibiotic substitute, a new antibacterial and anti-endotoxin double-effect peptide, which has high safety, strong antibacterial activity and endotoxin. Advantages of clinical development of new drugs. Related research results were published online on March 13 in Scientific Reports.
Wang Jianhua introduced that antibiotic resistance, drug residues and "super bacteria" appearing in recent years have sounded alarms for the use of antibiotics; there are side effects during the treatment - Gram-negative pathogen endotoxin lipopolysaccharide (LPS) release Directly threaten the health of the body. Therefore, the development of new antibiotic substitutes is imminent. At present, bovine lactoferrin-derived peptides, which have broad application potential in the food, medicine and feed veterinary medicine industries, have broad-spectrum bactericidal properties, but have high hemolytic properties and low biosafety.
The research team used the multi-amino acid combination site-directed mutagenesis technology to replace the three key sites of bovine lactoferrin-derived peptides from the core antibacterial sequence. The two mutants were more resistant to Staphylococcus aureus than the parent peptide. Methicillin-resistant Staphylococcus aureus (MRSA), Salmonella activity, and lower hemolytic activity. The study also found that mutants have a stronger ability to inhibit the synthesis of pathogenic bacteria such as DNA, RNA and protein. Animal experiments showed that injection of 10-15 mg/kg into infected mice significantly reduced the amount of pathogens in the body within 10 hours. In addition, the mutant can bind to bacterial endotoxin, inhibit the production of inflammation by reducing the level of serum pro-inflammatory factors in mice, reduce the induced damage of endotoxin to the lungs of mice, and significantly improve the survival rate of mice induced by endotoxin-induced toxemia.
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