Review Article

Therapeutic Potential of Human Amniotic Epithelial Cells on Injuries and Disorders in the Central Nervous System

Table 1

hAECs administered in animal models of injuries and diseases of the CNS and the possible mechanisms.

DiseasesAuthorsModel animalDelivery routeSuggested mechanismClinical improvement

Stroke[9]Acute ischemia ratsI.C.Reduced apoptosis
Neural differentiation
Reduced infarct volume
Improved functional behaviour
Stroke[32]
[34]
Acute ischemia mice and marmoset monkeysI.V.Reduced cerebral apoptosis and inflammation
Reduced systemic immunosuppression
Reduced infarct volume
Improved functional behaviour
Stroke[14]ICH ratsIntracerebralReduced microglial activation
Increased neural cell survival and regeneration
Reduced brain edema
Ameliorated neurologic deficits
Stroke[25]ICH rabbitsIntracerebralNeural differentiationImproved functional behaviour
Stroke[36]ICH ratsIntracerebralReduced microglial activation and inflammatory factorsReduced inflammation response
SCI[42]SCI monkeysInjected into the transection cavitiesPromote the growth of axotomized axons
Prevent the formation of glial scar
Prevented the formation of glial scar
Prevented death in axotomized cells
SCI[10]SCI ratsInjected into spinal transectionsPromote the regeneration of the axons
Inhibited the atrophy of axotomized red nucleus
Improved functional behaviour
SCI[43]SCI ratsInjected into spinal transectionsReduced microglial activationAlleviated SCI-induced mechanical allodynia
SCI[44]SCI ratsTransplanted into spinal transectionsEnhanced the survival of host neurons
Promoted the survival and neural differentiation of codrafted NSCs
Improved functional behaviour
SCI[46]SCI ratsTransplanted into spinal hemisections with muscle scaffoldPromoted axonal growth
Promoted the remyelination of nerve fibres
Improved functional recovery
SCI[47]SCI ratsTransplanted into spinal hemisections with silk fibroin scaffoldReduced the formation of glial scar
Reduced immunological reaction at lesion site
Improved functional behaviour
Parkinson’s[15]PD ratsIntracerebralPromoted the differentiation of the neurons expressing tyrosine hydroxylaseImproved functional behaviour
Parkinson’s[58]PD ratsIntracerebralPromoted the survival of dopamine neuronsImproved the survival of dopamine neurons
Parkinson’s[11]PD ratsIntracerebroventricularPrevented the loss of dopamine neurons and their metabolitesImproved behaviour recovery
Parkinson’s[59]PD ratsIntracerebralIncreased the content of dopamine neurons and their metabolitesImproved behaviour deficits
Alzheimer’s[12]
[65]
APP/PS1 miceIntracerebralIncreased survival of cholinergic neurons
Promoted acetylcholine production
Improved spatial memory
MS[13]EAE miceIntravenousSuppressed the proliferation of splenocytes and T cells
Increased proportion of Th2 production
Reduced demyelination
Ameliorated relapse and remission
MS[71]EAE miceIntravenousInhibited the proliferation of splenocytes
Increased the production of IL-2 and IL-5
Decreased remission
Demyelination
MS[72]EAE miceIntravenousIncreased the number of Treg and naïve CD4+ T cells
Decreased the T cell response and inflammatory factors
Ameliorated relapse
CP[52]Brain injury in preterm foetal sheepFoetal jugular veinReduced microglial activation, apoptosis and astrogliosis, and BBB integrity maintenanceProtected the developing brain
CP[51]Brain injury in preterm foetal sheepFoetal brachial arteryReduced microglial activation, pyknotic cells, and cell death
Increased oligodendrocytes and MBP-positive cells
Restored myelin morphology
Decreased white matter injury
CP[53]White matter injury in preterm foetal sheepIntravenous and intratrachealReduced microglial activation and vascular leakageModulated white matter pathology
CP[56]Brain injury in perinatal mouseIntravenousReduced apoptosis and astrogliosis
Increased microglial activity
Rescued the decreased body weight