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Postoperative complications are common issues that may arise from anesthetic drugs or surgical procedures. This study aimed to investigate the protective and therapeutic effects of ginsenosides on anesthesia-associated side effects and postoperative complications. This study was conducted following the PRISMA 2020 guidelines. A comprehensive search was conducted across PubMed/MEDLINE, Scopus, Web of Science, Embase, and the Cochrane Library to identify relevant studies published prior to October 13, 2024. Predefined inclusion and exclusion criteria were applied, and duplicates were removed. Ginsenosides inhibit oxidative stress and enhance cognitive function by activating pathways such as phosphoinositide 3-kinase (PI3K)/Protein kinase B (PKB) (AKT)/glycogen synthase kinase-3 beta (GSK-3β), promoting neuroplasticity, alleviating oxidative stress, and modulating neuroinflammatory markers, as well as microglia and astrocytes. They help to maintain mitochondrial integrity, thereby reducing apoptosis and neurotoxicity caused by anesthetic agents. Ginsenosides also alleviate postoperative pain by modulating N-methyl-D-aspartate (NMDA) and suppressing inflammatory cytokines. They also improved neuropsychological problems by increasing Nerve Growth Factor (NGF) and Brain-Derived Neurotrophic Factor (BDNF). The anti-fatigue properties of ginsenosides are attributed to enhanced antioxidant activity, improved skeletal muscle metabolic function, and increased Adenosine Triphosphate (ATP) production. These results are consistent with prior studies demonstrating the neuroprotective effects of ginsenosides. Despite promising outcomes, the prevalence of animal studies and the absence of clinical data underscore the necessity for clinical validation and safety profiling in future research. Preclinical evidence shows ginsenosides, particularly Rg1, Rb1, and Rg3, demonstrate promising protective and therapeutic effects against anesthesia-associated adverse effects and postoperative complications. Show less

Pharmacogenomics (PGx) is a scientific field that aims to understand how an individual's genetic code regulates drug metabolism and response. The response to many anesthetic drugs varies widely among patients due to many factors including, but not limited to, age, gender, and comorbidities. However, PGx contributes to this variability, particularly regarding adverse drug reactions. This review explores the influence of PGx on five commonly used induction agents in anesthesia: propofol, midazolam, ketamine, etomidate, and thiopental. Propofol metabolism is significantly affected by polymorphisms in CYP2B6, CYP2C9, and UGT1A9, influencing both efficacy and toxicity. Midazolam's PGx is mainly mediated by variations in CYP3A4, CYP3A5, and UDP-glucuronosyltransferase enzymes, with implications for sedation depth and drug clearance. Ketamine response is modulated by polymorphisms in metabolic enzymes (e.g. CYP2B6), as well as neurobiological targets such as brain-derived neurotrophic factor and gamma-aminobutyric acid (GABA) receptors, particularly in psychiatric applications. Etomidate shows less studied but emerging PGx associations, including single-nucleotide polymorphisms in GABA receptor subunits and metabolic enzymes, which may affect both sedative depth and cardiovascular stability. Thiopental is a rapid-acting metabolite whose effect stems from GABA-A receptor potentiation; no studies have yet identified specific genetic polymorphisms influencing its action. Overall, PGx provides a promising avenue for tailoring anesthetic management to improve patient safety and outcomes. However, clinical integration remains limited due to practical and infrastructural barriers. This review highlights the potential and current limitations of pharmacogenomic-guided anesthesia, underscoring its relevance in the era of precision medicine. Show less