Table 6.

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

Model	Type	Tissue sites	Effects	Mechanisms	RF
MCAO in rats	In vivo	Ischemic stroke	↓ mortality rates ↓ t-PA-mediated BBB disruption ↓ hemorrhagic transformation	Scavenge peroxynitrite ↓ MMP-9 expression and activity ↓ Peroxynitrite-mediated MMP-9 activation	[147]
STZ injection aggravated the brain damage induced by MCAO surgery OGD/REP-induced P12 cells	In vivo In vitro	Cerebral I/R injury	↓ blood glucose, neurological deficit, and infarct volume ↓ ROS production and Drp-1 expression ↓ mitochondrial fission ↑ mitofusin-2 (MFN2) generation ↑ Drp-1 Ser637 phosphorylation ↑ mitochondrial membrane potential	↓ cell apoptosis ↑ mitophagy Regulating mitochondrial functions in an AMPK-dependent manner	[151]
Global cerebral I/R in gerbil OGD-induced SH-SY5Y cells	In vivo In vitro	Ischemia-induced memory impairment	↑ learning and memory impairment ↓ intracellular calcium concentration ↓ phosphorylation level of CaMKII ↓ caspase-3 and Bax expression ↑ Bcl-2 expression	↓ phosphorylation level of CaMKII ↓ hippocampal neuronal apoptosis	[149]
Hypoxic-ischemic encephalopathy in rats	In vivo	Hypoxic-ischemic injury	↓ cerebral infarct volume ↓ neuronal loss ↓ apoptosis ↑ p-AKT and glutamate transporter 1 expression	↑ glutamate transporter 1 via the PI3K/AKT signaling pathway	[150]
MCAO in rats	In vivo	Cerebral ischemic injury	↓ neurological deficits ↓ infarct volume ↑ NeuN, GFAP, and progesterone receptor expression	↑ progesterone and adrenocorticotropic hormone expression	[152]
MCAO/R in rats OGD/R-induced primary astrocytes	In vivo In vitro	Acute ischemic stroke	↓ SDH level ↓ glutamine synthetase loss ↓ ROS production	↓ ROS production ↓ excitotoxicity ↑ glutamate disposal ↓ oxidative stress	[148]

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