New Insights into CAZ-AVI’s Pharmacological Mechanisms: Network Pharmacology and Molecular Docking Reveal Molecular Targets in Pneumonia Treatment

Abstract

Ceftazidime-Avibactam (CAZ-AVI) has demonstrated good efficacy in treating pneumonia. Currently, research on CAZ-AVI is primarily focused on its direct antibacterial effects, while exploration of its potential host targets remains relatively limited. In light of this, our study innovatively employs a research strategy that integrates network pharmacology and computer-aided drug design to systematically explore the potential host targets of CAZ-AVI. We identified 141 intersecting targets in CAZ-AVI-treated pneumonia, with key targets including Epidermal Growth Factor Receptor (EGFR), Src Proto-Oncogene (SRC), Signal Transducer and Activator of Transcription 3 (STAT3), Heat Shock Protein 90 Alpha Family Class A Member 1 (HSP90AA1), Caspase 3 (CASP3) and Nuclear Factor Kappa B Subunit 1 (NFKB1). By inhibiting or activating these target proteins, CAZ-AVI plays a significant regulatory role in cell proliferation, apoptosis, signal transduction, and immune responses. Our experimental results further confirmed that the compound possesses activities in inhibiting cell proliferation and promoting apoptosis. CAZ-AVI can correct cellular dysfunction and optimize immune responses, thereby providing new strategies and insights for the treatment of pneumonia.