In the current study, we demonstrated that SDSS has neuroprotection effect on cerebral ischemia and reperfusion injury following in a rat MCAO
model, as it improved neurologic deficits and survival, reduced infarct volume and increased the number of viable neurons on day 5 after MCAO
We used the rat MCAO
model of stroke to study brain damage.
At 48 hours after MCAO
, there was a significant loss of miR29b at the infarct site.
In this study we found that vitexin effectively reduced cerebral infarct volume and ameliorated neurological deficit and histopathological damage in a preclinical mouse MCAO
So, Dragon's blood dropping pills had protective effects and improved the antioxidant activity of MCAO
rats on scavenging excessive free radicals and decreasing lipid peroxidation.
The aim of the present study was to determine whether these components could be reliably measured in MCAO
Focal cerebral ischemia was induced by MCAO
as described previously by Longa et al.
In vivo studies showed that melatonin treatment after MCAO
significantly inhibited inducible NOS activity and attenuated expression of the inducible isoform, resulting in decreased total NOS activity and tissue nitrite levels.
is extensively accepted as a model of brain injury in vivo.
Male Sprague-Dawley rats were anesthetized and subjected to 2 hours of MCAO
followed 24 hours reperfusion.
The rats were decapitated under halothane anesthesia, the brain was removed rapidly and dissected 24 h after MCAO
, tissue samples from the ischemic hemisphere were weighed immediately on preweighed aluminum foil to determine the yield of wet tissue.
The protective OR treatment with AGE prevented the increase in nitrotyrosine and the decrease in total superoxide dismutase, glutathione peroxidase, and extracellular superoxide dismutase activities induced by MCAO