Yiqihuoxue Compound Sxd Experimental Study Inhibition Of The Inflammatory Reaction Of Acute Cerebral Infarction

Objects: To investigate the effect of "tonifying qi and moving blood" formula on acute cerebral infarction inflammation response and apoptosis of nerve cell by detecting the changes of tumor necrosis factor- a , intercellular adhesion molecular-1(ICAM-1), nuclear factor k B(NF- k B),caspase3 in brain and leucocyte Adhesion molecule CD11/CD18 in blood after cerebral ischemia,Methods: Electrocoagulation method to occlude middle cerebral artery of rat to make the MCAO rat model. Give SXD 8 days before making model, one time each day. MCAO rat model are dvided into 4 groups randomly as following: High dose SXD group; Middle dose SXD group; Low dose SXD group; Cyclophosphamide (Cytoxan) group. Sham operation group, Model group, and Normal group as control groups. After making model, the intervention period are 24 hours, 48 hours and 72 hours respectively. In this case, the infarct pathology alteration can be observed by noticing the change in HE, Nissl body change by Nissl's staining, infarct volume detected by TTC staining, CD11a/CD18,CD11b/CD18 in leucocyte detected by flow cytometry, expression of ICAM-lmRNA detected by RT-PCR, expression of NF- k Band caspase 3 tested by Immune histochemistry method.Results: SXD have the function of decreasing the volume size of cerebral infarction and of protecting neuron. They can dramatically lower the expression of TNF-a m-RNA and that of adhesion molecular CD11a/CD18 CD11b/CD18 and ICAM-1 m-RNA, It also restrain the activation and expression of NF- k B. The function of the above high dose group is similar to the effect of Cytoxan. SXD and Cytoxan can decrease the expression of caspase3, and the effect of high dose SXD is better than Cytoxan group.Deferent dosage SXD and stable dosage cyclophosphamide can control theexpression the integrate of ICAM-land CD11/CD18 and adhesiveness of leucocytes and blood vessel endothelial cell, can relieve the collection and infiltration of inflammation cell, can tissue infiltration and brain damage due to ischemia by regulate down theexpression of TNF- a mRNA, restrain the activation and activity of NF- k B, decrease the expression of ICAM-1mRNA and CD11/CD18. On the other hand, SXD and cyclophosphamide can restrain the apoptosis after cerebral ischemia by control the expression of TNF- a mRNA and caspase 3.The experiments use active components of SXD to explore the herb function of inflammation in the early period of acute cerebral infarction, and, for the first time, prove the anti-inflammation role. We also research the influence on cytokine TNF- a after cerebral ischemia at gene level first. Further more, the experiments also include the influence on NF- k B during cerebral ischemia process and the influence on caspase 3, which is the key protease of apoptosis after cerebral ischemia. The experiments suggest that the anti-inflammation role after cerebral ischemia is an active mechanism of tonify qi and many move blood formula and part of move blood herb, which needs further confirmation. We are putting forward that the adhesiveness of leucocytes and endothelial cell, inflammation cell aggregation and infiltration, micro vessel blockage are among the basic pathological phenomena of "blood stasis" of traditional Chinese medicine; this hypothesis has certainly enriched the connotation of blood stasis of TCMConclusions: The results indicate that SXD can inhibit MCAO model rat inflammation response in early stage of infarct, decrease the pathological damage after cerebral ischemia, and restrain the apoptosis of nerve cell.Anti-inflammation of cerebral infarction in early stage maybe one of the activemechanism of tonify qi and move blood formula or part of move blood herbs. The adhesiveness of leucocytes and endothelial cell, the collection, infiltration of inflammation cell and blockage of micro vessel is one of pathology basis of "blood stasis" of TCM.