Abstract
Hypoxia-ischemia (HI) is one of the most common causes of death and disability in neonates. Currently, the only available licensed treatment for perinatal HI is hypothermia. However, it alone is not sufficient to prevent the brain injuries and/or neurological dysfunction related to HI. Perinatal HI can activate the immune system and trigger the peripheral and central responses which involve the immune cell activation, increase in production of immune mediators and release of reactive oxygen species. There is mounting evidence indicating that regulation of immune response can effectively rescue the outcomes of brain injury in experimental perinatal HI models such as Rice-Vannucci model of newborn hypoxic-ischemic brain damage (HIBD), local transient cerebral ischemia and reperfusion model, perinatal asphyxia model, and intrauterine hypoxia model. This review summarizes the many studies about immunomodulatory mechanisms and therapies for HI. It highlights the important actions of some widely documented therapeutic agents for effective intervening of HI related brain damage, namely, HIBD, such as EPO, FTY720, Minocycline, Gastrodin, Breviscapine, Milkvetch etc. In this connection, it has been reported that the ameboid microglial cells featured prominently in the perinatal brain represent the key immune cells involved in HIBD. To this end, drugs, chemical agents and herbal compounds which have the properties to suppress microglia activation have recently been extensively explored and identified as potential therapeutic agents or strategies for amelioration of neonatal HIBD.
Highlights
Neonatal hypoxic-ischemic brain damage (HIBD) is the leading cause of death and long-term neurological deficits in infants and children
In a newborn rat HIBD model by Rice-Vannucci method and lipopolysaccharide, after using FTY720 at 0.3 mg/kg by intraperitoneally injection within 30 min after HIBD to eliminate lymphocytes, the results showed an obvious reduction of neuroinflammatory reaction, and the incidence of cerebral palsy was decreased coupled with recovery of the motor function (Yang, 2014)
There is compelling evidence indicating that regulation of immune response involving microglia, monocytes and lymphocytes can effectively rescue the outcomes of brain injury in which apoptosis of neurons is featured prominently in experimental perinatal hypoxic ischemic model
Summary
Neonatal hypoxic-ischemic brain damage (HIBD) is the leading cause of death and long-term neurological deficits in infants and children. Studies have found that in a rat ischemia-reperfusion model, mannitol reduces NO expression and apoptosis in the brain, thereby reducing the damage to cell structure, cerebral infarct size and behavioral deficit after HIBD (Chen, 2018).
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