Acomplexcascadeofmoleculareventsisconsiderdtobeinitiatedfollowingcerebralis chemia ,whichincludereleaseofexcitatoryaminoacid ,calciumdyshomeostasis ,freeradicalinjury ,increased cytokines,caspaseactivationandalteredgeneexpression .Thisreviewprovidesanoverviewofmolecular mechanismsinvolvedinpostischemicneuronaldeathandanalysesthepotentialfortherapeuticintervention .

Oxidative stress has been implicated in brain injury after ischemia, which is a complex cascade. These oxidants produced by oxidative stress are directly involved in oxidative damage with cellular macromolecules such as lipids, proteins and nucleic acids, which lead to cell death. Oxidants are also mediators in signaling involving mitochondria pathway, DNA repair enzymes, and transcription factor that may lead to apoptosis after cerebral ischemia. Antioxidangt enzymes (such as superoxide dismutase,etc) provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury. This review focuses on the mechanisms of oxidative stress during brain ischemia.

In this study we found that while pituitrin induced a significant decline of nutritional blood flow of myocardium in mice, oxygen free radical concentration andmalondialdehyde content significantly increased, and superoxide dismutase activity signifi-cantly declined in the ischemic myocardium. These results suggest that this pituitrin-inducedmyocardial ischemia in mice may serve as an easy-to-operate, cheap and in vivo model forscreening oxy-radical scavengers in the study of anti-ischemic myocardial injury.

Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.

Cell protection from stresses by heat shock protein (HSP) was previously attributed to its ability to prevent aggregation and to accelerate refolding of damaged proteins. It plays an important role in cell survival after extremely harsh protein damaging treatment leading to necrotic cell death. On the other hand, protein repair function of HSP cannot explain how it protects cell from stresses which do not cause direct protein damage. These stresses kill cell through activation of apoptotic program. Recently it has been found that HSP can meditate suppression of a stress-activated protein kinase, JNK, an early component of stress-induced apoptotic signaling pathway.These observations can provide a basis for HSP's function of anti-apoptosis.

C. Conclusion The optimal SINI TANG composition comprises three active components combined at clinical maximal dosage showed the best therapeutic efficacy, of which A is a key factor and B, C are necessary factors for the composition in SINI TANG.

To explore the presence of informative protein biomarkers in the salivary proteome of breast cancer patients with thick white or thick yellow tongue fur.

Effects of Sini decoctiou (SD ) on ischemic (anoxic ) electrocardiogram (ECG ) and possible action mechanism of SD were studied.Results indicate that SD significantly improves the pituitrin induced ischemic ECG of rabbits, significantly prevents S-T scgment from desconding and suppresses the elevation of T wave; SD can also lengthen significantly cardioe lectric activity time of anoxic mice. The protective cffects of SD on ischemic (anoxic ) myocardium may be related to the significant increase of myocardial nutritional blood flow induced by administrating SD.

Objective Investigate the relation between decrease of apoptosis caused by delayed preconditioning and expression of SMAC and XIAP.Methods Sprage-Dawleyt rats were divided into four groups: control,sham,I/R and IPC/SWOP.The rats in I/R group underwent ischemia for 1 hour by classic artery ligation and reperfusion for 1 hour.The rats in IPC/SWOP group underwent tree cycles of 5-minute ischemia and 5-minute reperfusion 24 hours prior to the index occlusion.Cell apoptosis was measured by flow cytometry,the activity of caspase-3 was also measured.The expression of SMAC and XIAP in cytosol of myocardial cell was measured by Western blot.Results Cell apoptosis rate,activity of caspase-3 and expression of SMAC significantly increased in I/R as compared with control(P