Penehyclidine hydrochloride can promote microcirculation and reduce vascular permeability. However, the role of
penehyclidine hydrochloride in
cerebral ischemia-
reperfusion injury remains unclear. In this study, in vivo
middle cerebral artery occlusion models were established in experimental rats, and
penehyclidine hydrochloride pretreatment was given via
intravenous injection prior to model establishment. Tetrazolium
chloride,
terminal deoxynucleotidyl transferase-mediated
deoxyuridine triphosphate-
biotin nick end labeling and immunohistochemical staining showed that,
penehyclidine hydrochloride pretreatment markedly attenuated neuronal histopathological changes in the cortex, hippocampus and striatum, reduced
infarction size, increased the expression level of Bcl-2, decreased the expression level of
caspase-3, and inhibited neuronal apoptosis in rats with
cerebral ischemia-
reperfusion injury.
Xanthine oxidase and
thiobarbituric acid chromogenic results showed that
penehyclidine hydrochloride upregulated the activity of
superoxide dismutase and downregulated the concentration of
malondialdehyde in the ischemic cerebral cortex and hippocampus, as well as reduced the concentration of extracellular
excitatory amino acids in rats with
cerebral ischemia-
reperfusion injury. In addition,
penehyclidine hydrochloride inhibited the expression level of the NR1 subunit in hippocampal nerve cells in vitro following
oxygen-
glucose deprivation, as detected by PCR. Experimental findings indicate that
penehyclidine hydrochloride attenuates neuronal apoptosis and oxidative stress injury after focal
cerebral ischemia-reperfusion, thus exerting a
neuroprotective effect.