TABLE 2.

Summary of neuroprotective agents for infection-sensitised neonatal brain injury.

Agent	Preclinical evidence
Histone deacetylase inhibitor (HDACi) trichostatin A (TSA)	Reduces white and grey matter injury, and cell death improves inflammatory profile and long-term learning in the mouse (Liu et al., 1989; Brogdon et al., 2007; Suh et al., 2010; Yakovlev et al., 2010; Fleiss et al., 2012).
Plasminogen activator inhibitor-1 (PAI-1 – CPAI)	Decreases brain damage, BBB damage, and inflammation via reduction of microglia activation and modulation of anti-inflammatory pathways in the rat (Zhang et al., 2007; Yang et al., 2009).
Cell-penetrating anti-NF-κB peptides (Tat-NBD)	Downregulates microglial activation and NfkB in the rat (May et al., 2000; Pizzi et al., 2009).
FTY720 (fingolimod) – sphingosine-1-phosphate receptor agonist	Reduction in IL-17A-positive lymphocytes, lower levels of pro-inflammatory cytokines, attenuated BBB damage, and protected brain white matter and motor development.
Vancomycin – Gram-positive bacterial infection	Downregulate LPS-induced TNF-α production (Siedlar et al., 1997) whilst upregulating anti-inflammatory, IL-10, cytokine production (Ziegeler et al., 2006).
Properdin	Reduces cell death, microglial activation (Sisa et al., 2019a).
Glucocorticoids	Prolonged administration of dexamethasone has been implicated in increased cell death (Whitelaw and Thoresen, 2000). Hydrocortisone administered both decreased infarction size (Harding et al., 2017).
N-acetylcysteine	Decreases acute brain edoema and sub-acute brain atrophy in a rodent model (Xu et al., 2005).
Downregulation of microRNA-21 (miR-21)	Increases caspase activity and lipid peroxidation in a rodent model injury (Wang et al., 2007b).
PTEN-induced putative kinase 1 (PINK1)	Attenuated brain infarct volume 24 and 72 h post insult, reduced cell death (Zhu et al., 2016).