The Experimental Study Of HuangJiao Grain On Acute Cerebral Ischemic Neuronal Apoptosis On Rats

Objective: To prevent and treat cerebral ischemic neuronal apoptosis was a highlight of study in treating acute cerebral infarction(ACI). HuangJiao grain (HJG)have gain good effect on ACI according to clinical research. In order to investigate the possible mechanism, the experiment were done.Methods: Animals and groups: Sixty older Wister rats were randomly divided into six groups: normal group, Nimodipine control group , model group, HJG lowest group, HJG moderate group and HJG maxim group. Methods of administration and treatment: On the 30minture Before mold making ,Rats of nimodipine group ,model group, HJG lowest group, HJG moderate group and HJG maxim group were to be administed respectively at dose of 10g/kg,5g/kg,2. 5g/kg of 100%, 50%, 25% HJG mixture, imodipine group at dose of 10mg/kg to 1% Nimodipine mixture, normal group and model group at dose of 10ml/kg saline mixture. Separation and detection methods: After 24 hours, put mice to death by stretch neck, sprated brain, and detected bcl-2,bax,fas and caspase-3 antigen distribution in brain by immunohistochemistry, observed brain microstrueture by HE staining, observed brain ultrastrueture by transmission election microscope, detected the neuronal apoptosis in brain by terminal deoxynucleotidy 1 transferase mediated dUTP-biotin nickend labeling (TUNEL ),took blood 4ml to measure the change of superoxide disutase (SOD), malondiadehyde (MDA),Tumor necrosis factor-a(TNF-a)and N0(nitric oxide). Statiscal method: Differences between groups were compared by Q-test and F-test.Result1 Compared with the normal group, the level of TUNEL, bax, NO, MDA, fas, bc1-2, Caspace-3 expression level of model group increasedsignificantly ( all P<0. 01) , the levels of SOD, bcl-2/bax decreased significantly (all P<0. 01) .2 Compared with the model group , the level of TUNEL,bax, NO, MDA, fas, Caspace-3 of HJG lowest group, HJG moderate group, OHJG maxim group and Nimodipine group decreased significantly (P<0. 05,P<0. 01), the level of bcl-2,SOD and bcl-2/bax increased significantly (P<0. 05 , P<0. 01).3 Compared with the Nimodipine control group, the level of NO of HJG maxim group decreased significant1y (P<0. 05) , the level of SOD and bcl-2/bax increased significantly(P<0. 05, P<0. 01); the level of TUNEL, bax, fas ,MDA, Caspace-3 was insignificantly (P>0. 05) .4 Compared with HJG maxim group, the level of TUNEL,bax,NO, MDA, fas, Caspace-3 of HJG lowest and moderate groups increased significant ly (P<0. 05,P<0. 01), the level of bc1-2,SOD and bcl-2/bax decreased significantly (all P<0. 01) .5 Microstrueture and u1trastrueture of brain appear notable apoptosis after acute cerebral ischemic. Different-dose HJG can relieve the apoptosis of brain cells.Conclusion : Acute cerebral ischemic can result in neuronal apoptosis ,which have been demonstrated by different level (morphological strueture, ce11, protein and gene).HJG has signify-cantly protective effect on neuronal apoptosis , and the effect was better than Nimodipine. The possible mechanism was due to decrease of the level of TUNEL, bax, NO, MDA, fas, Caspace-3 and increase the activity of SOD and be 1-2.