Table 3.

Summarized effects and mechanisms of Rg1 on different targets related to ischemic stroke in in vivo and in vitro studies.

Model	Type	Tissue sites	Effects	Mechanisms	RF
d MCAO in mice OGD-induced hCMEC/D3 cells	In vivo In vitro	Ischemic stroke	↑ neurobehavioral outcomes ↓ brain infarct volume ↑ CD31 expression ↑ BrdU+/CD31+ microvessels ↑ GFAP-positive vessels ↑ proliferation, migration, and tube formation of endothelial cells	↑ VEGF, HIF-1α, PI3K, p-AKT, and p-mTOR expression ↑ PI3K/AKT/mTOR signaling pathway	[85]
t MCAO in rats OGD/R-induced PC12 cells	In vivo In vitro	I/R-induced neuronal injury	↓ cell injury ↓ MiR-144 activity Prolong Nrf2 nuclear accumulation ↑ Nrf2 transcriptional activity ↑ ARE-targeted genes expression	↓ oxidative stress ↑ Nrf2/ARE Pathway ↓ MiR-144 activity	[86]
MCAO in mice	In vivo	Cerebral I/R injury	↓ infarct volume ↓ neurological deficit scores ↓ IL-1ß, TNF-α, and IL-6 contents ↓ Glu and Asp contents	↑ BDNF expression ↓ IL-1ß, IL-6, and TNF-α expression ↓ Glu and Asp contents	[89]
OGD-insulted NSCs	In vitro	Ischemic stroke	↓ NSC viability ↓ OGD-induced apoptosis ↓ cleaved caspase-3 and Bax expression ↑ Bcl-2 expression	↓ oxidative stress ↓ p38/JNK2 phosphorylation	[87]
MCAO/reperfusion in rats	In vivo	Cerebral I/R injury	↑ neurobehavioral function ↓ infarct volume ↓ BBB permeability	↓ PAR-1 expression	[88]
MCAO in rats	In vivo	Cerebral I/R injury	↓ infarct volume ↓ neurological deficit ↓ proinflammatory cytokine expressions ↓ proteasomal activity ↓ protein aggregate accumulation	↓ NF-κB nuclear translocation ↓ IκBα phosphorylation ↓ ubiquitinated aggregates ↓ inflammatory response	[90]

RF: reference; other abbreviations as shown in the literature. (↓): downregulation or inhibition; (↑): upregulation or activation.