**Table 2.**

*Neuroprotection - New Approaches and Prospects*

cerebral cortex neurons

[112] SH-SY-5Y cells 6 h OGD/ 1 h

Cortical Neuron

progenitor cell

hippocampal neurons HT22

and primary murine cortical neurons,

astrocytes and microglial cells

astrocytes

hippocampal neurons

myeloma cell line U266

leukemic cell lines NB4 and U937

glioblastoma cell line

cell lines U373MG and DBTRG05MG

[81] Neuro 2a cells 4 h OGD/ 12 h

astrocyte

[111] Primary cortical neurons

[76] Primary

[79] Primary

[77] Primary

[78] Neural

[113] Mouse

[114] SH-SY5Y cells

[115] Primary

[116] Primary

[117] Primary

[82] Multiple

[83] Myeloid

[118] U251 human

[119] Glioblastoma

HMAs models

**Reference Species Animal model Outcomes**

3 h OGD/ 48 h Reperfusion

3, 5, 7 h OGD/ 24 h Reoxygenation

reoxygenation

4 h OGD/ 24 h Reoxygenation

Reoxygenation

2 h OGD/ 48 h Reoxygenation

2 h OGD/ 24 h reperfusion

Reference Cell line/species Experimental model Outcomes

4 h OGD/ 3 h, 6 h, 12 h, 24 h reoxygenation

Damage to neuronal viability, dendrite branch number in neurons deceased

Increases in HMGB1 and TNF-a, induced phosphorylation of PI3K, promoted nuclear translocation of NF-kB

Caused significant mitochondrial fragmentation, excessive mitochondrial

miR-144-3p expression was significantly downregulated in neurons following

depolarization, reactive oxygen species production, lipid peroxidation and DNA

Induced abnormally opened hemichannels with increased ATP release and EtBr uptake but reduced GJIC permeability. Astrocytic Cx43, hemichannels, and GJIC play critical roles in OGD/R injury-induced

significantly

2 h OGD Suppressed significantly cortical neurons proliferation

OGD/R treatment

Inhibited cell viability and cell proliferation, reduced phosphorylation levels of p38 MAPK and ERK1/2

neuroinflammatory responses.

Expression of Ski was proved to be

Caspase-3 activity and expression increased in the first 24 h,

expression profiles of genes that are functionally related to apoptosis and

transmembrane potentials, activation of caspase-3/8 and cleavage of anti-apoptotic

degradation and invasion of glioma cells

fission

OGD Decrease in neurite outgrowth

4 h OGD OGDR-induced mitochondrial

damages

up-regulated

CoCl2 CoCl2-mediated hypoxia affects the

angiogenesis

protein Mcl-1

DFO Activation of factors associated with ECM

CoCl2 Increases HIF-1a gene expression

CoCl2 and DFO Apoptosis with a loss of mitochondrial

6 h OGD Increased apoptosis

**218**

*Experimental models for HI.*
