Objective:To explore the network control mechanism of the calcium signaling pathway in cerebral ischemic injury after intervention by the main components of Qingkailing(清开灵),i.e.Baicalin,Jasminoidin and their combination.Methods:Thirty mice were randomly divided into 5 groups,a baicalin group,a Jasminoidin group,a baicalin plus Jasminoidin group,a nimodipine group,and a model group(n=6).The global cerebral ischemia-reperfusion mouse model was established.The mice were administrated respectively by injection of baicalin,Jasminoidin,mixture of baicalin and Jasminoidin,and nimodipine into the caudal vein,with the model group given no any drug.Three hours after operation,the brain was removed and sectioned.After calculation of cerebral ischemic area by 2,3,5-triphenyltetrazolium staining,the percentage of infarct volume was calculated.The total RNA of the mouse brain tissue was extracted to obtain the whole genome expression profile,and the differentially expressed genes related to the calcium signaling pathway was analyzed with Bayesian network structures.Results:Compared with the model group,the ischemic area was significantly reduced in the baicalin group,the Jasminoidin group,the Baicalin plus Jasminoidin group(all P<0.05).The ischemic area in the baicalin plus Jasminoidin group was smaller than the other three groups(all P<0.01).In the gene regulatory network structures of calcium signaling pathway,the average length and equitability were the highest in the baicalin plus Jasminoidin group,followed by the nimodipine group.Conclusion:Compared with a single component,combination of Baicalin and Jasminoidin can more obviously intervene in the overall expression of calcium signaling pathway,and the mechanism is related with the aggregation characteristic of the gene expression network. Objective: To explore the network control mechanism of the calcium signaling pathway in cerebral ischemic injury after intervention by the main components of Qingkailing, ie Bioin, Jasminoidin and their combination. Methods: Thirty mice were randomly divided into 5 groups, a baicalin group, a Jasminoidin group, a baicalin plus Jasminoidin group, a nimodipine group, and a model group (n = 6). The global cerebral ischemia-reperfusion mouse model was established. The mice were administrated separately by injection of baicalin, Jasminoidin , mixture of baicalin and Jasminoidin, and nimodipine into the caudal vein, with the model group given no any drug. Three hours after operation, the brain was removed and sectioned. After calculation of cerebral ischemic area by 2,3,5-triphenyltetrazolium staining , the percentage of infarct volume was calculated.The total RNA of the mouse brain tissue was extracted to obtain the whole genome expression profile, and the differentially expressed genes related to t The calcium signaling pathway was analyzed with Bayesian network structures. Results: Compared with the model group, the ischemic area was significantly reduced in the baicalin group, the Jasminoidin group, the Baicalin plus Jasminoidin group (all P <0.05). ischemic area in the baicalin plus Jasminoidin group was smaller than the other three groups (all P <0.01). In the gene regulatory network structures of calcium signaling pathway, the average length and equitability were the highest in the baicalin plus Jasminoidin group, followed by the nimodipine group . Conlusion: Compared with a single component, combination of Baicalin and Jasminoidin can more obviously intervene in the overall expression of calcium signaling pathway, and the mechanism is related with the aggregation characteristic of the gene expression network.