Intervention Of Breviscapine On The Expression Of Bcl-2/Bax In Rats' Hippocampus After Cerebral Resuscitation

Objective: To investigate the expression of Bcl-2/Bax in hippocampus after the Breviscapine (Br) intervention therapy the Sprague-Dawley(SD) rats with global cerebral ischemia/reperfusion (I/R) injury and testify the effect mechanism of Br during cerebral resuscitation. Methods: 72 healthy SD rats were randomly divided into 3 groups: sham operation (SO) group (n=24), I/R group (n=24) and Br group (n=24).Then each group were assigned into 4 observing time-points:3, 12, 24 and 48 hours (h) according to reperfusion time. The SD rats model of global cerebral ischemia/reperfusion (including: I/R and Br group) was produced by means of simple Pulsinelli-Brierley's four arteries occlusion method. SO and I/R groups were intraperitoneally injected with 0.9% Sodium Chloride (dose: 1ml/kg), and Br group with Breviscapine (dose: 2.5 mg/kg) one time per six hours. Then SD rats' cerebrums were taken out of their skull at each observing time-point. The expression activation of Bcl-2/Bax in pyramidal cells in hippocampus cornu ammonis (CA)1 region were examined by immunohistochemical method (SABC), measure average Grey value; hematoxylin and eosin (HE) staining was also performed to detect the number of surviving pyramidal cells, and terminal-deoxynucleotidy transferase medated dUTP nick end labeling (TUNEL) was used to detect apoptotic pyramidal cells (positive cells). Results: The expression activation of Bcl-2 began to decrease at 3h after reperfusion, The expression activation of Bax began to decrease at 3h after reperfusion, 12h continue decreasing, decreased to the peak at 24h, and then gradually increased. But , with the reperfusion prolonged, the number of surviving neurons became more and more lower (all P<0.01), and more and more neurons emerged the phenomenon of cell-apoptosis, its apoptotic pyramidal cells then clearly rised, too(all P<0.01). In Br group, the expression of Bcl-2 did decreased at 3h after reperfusion, significantly decreased at 12h and then gradually increased, average Grey value of Bax did significantly decreased at 3h after reperfusion(all P<0.01). Breviscapine after the intervention of Bcl-2 average Grey value at each time point were all significant lower than I/R group after reperfusion(all P<0.01), Bax average Grey value at each time point were still obviously higher than I/R group after reperfusion(all P<0.01). Conclusions: After global cerebral ischemia/reperfusion, Breviscapine could protect the brain from global cerebral ischemia/reperfusion injury by holding up the expression activation of Bcl-2/Bax, inhibiting neuronal apoptosis, increasing the number of surviving neurons. Breviscapine 12 hours is the role of decision that hippocampus cornu ammonis (CA)1 region neurons is survival time.