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EE is an intensive intervention ( Anti-apoptotic drugs High expression of the pro-apoptotic protein p53 in NSCs leads to disruption of endogenous neurogenesis after neonatal HIBD ( Anti-inflammatory drugs Neuroinflammation has been demonstrated to inhibit neurogenesis and the presence of various inflammatory components, such as immune cells, cytokines, or chemokines, plays a role in regulating the survival, proliferation, and maturation of NSCs ( via blocking microglia activation, which may also apply to neonatal HIBD, because neuroinflammation is also one of the important injuries mechanisms of neonatal HIBD ( Endogenous growth factor analogues Numerous growth factors can increase the proliferation of endogenous NSCs under a variety of conditions, thus promoting the endogenous neurogenesis process
