RESUMO
Aim To investigate the effects of baicalin on cognitive function in global cerebral ischemia reper-fusion rats, and the probable mechanism involved. Methods Sixty male Sprague-Dawley(SD) rats were randomly divided into Sham operation group ( S group) , global cerebral ischemia reperfusion group ( I/R group) , global cerebral ischemia reperfusion + ba-icalin treatment group ( I/RB group) , twenty in each. Model was induced via the bilateral occlusion of the common carotid arteries plus hemorrhagic hypotension. 12 h after reperfusion, rats in I/RB group were given baicalin (100 mg·kg-1 ) saline solution by intragas-tric administration twice per day for 7 days. Rats in S group and I/R group were given the corresponding dose of saline infusion at the same time. Morris water maze test was employed to detect spatial learning and memo-ry. BrdU immunohistochemistry was used to detect the proliferation of neural precursor cells ( NPCs ) in the brain. Expression of COX-2 in the brain tissue was measured by Western blot. Results Compared to I/R group, baicalin improved spatial learning and memory damage ( P nitive function in the rats with global cerebral ischemia reperfusion, which might be associated with its inhibi-tory effects on the expression of COX-2 , thereby in-creasing the proliferation of NPCs in the brain.
RESUMO
Aim To study the protective effects of Rhynchophyll a of total alkaloids ( RTA ) on cerebral ischemia/reperfusion injury and the possi ble mechanism of action. Methods The effects of RTA on decapit ated gasping model and model of middle cerebral artery ischemia 2 h/reperfusion 22 h were observed. The neurological scores, cerebral infarct volume and cerebr al water content after ischemia/reperfusion were observed in rats respectively. The activities of NOS and SOD and the content of MDA in rat's brain tissue were measured. Neuron apoptosis in ischemia penumbral area were detected by terminal depoxynucleotidyl transferase mediated dUTP-biotin nick end labeling ( TUNEL ) . Results The average gasping times in mice treated with RTA 50 , 75 mg?kg -1 was significantly prolonged. The cerebral infarct volume and cerebral water content in rats treated with RTA 40, 60 mg?kg -1 were sign ificantly decreased in ischemic rats. RTA 40, 60 mg?kg -1 increased the ac tivity of SOD ,and decreased the activity of NOS and the content of MDA in the i schemic brains of rats. The number of apoptotic neurons in ischemia penumbral ar ea of cerebral tissue of rats treated with RTA 40, 60 mg?kg -1 was signif icantly lower than that in control rats. Conclusions RTA has pr otective effect on cerebral ischemia/reperfusion injury; this may be related to inhibit the activity of NOS and lipoperoxidation, and increasing the activity of SOD and decreasing neuron apoptosis.