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.

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.

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.

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.

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

Therapeutic method is an important component of traditional Chinese medicine theory. Research on warming therapy focuses on pharmacology at present. Studying the feature of nerve-body fluid-metabolism-function in cold syndrome is of importance for illustrating the nature of warming therapy and elucidating the function of medication. This review presents the research and development of warming therapy in order to provide enlightenment for the research of therapeutic method from the aspects of traditional Chinese medicine and western medicine.

AIM: To compare effects of SiNi-decoction and Vitamin E on vascular endothelial function of experimental atherosclerosis rabbits and their therapeutic action on atherosclerosis. METHODS: The model of experimental atherosclerosis rabbits fed with forage of high lipid was established and treated in groups randomly. At the end of the experiment, samples of aorta and blood were taken and the percentage of lipid plaque area of aortic endothelium ,lipid metabolism and vascular endothelial oxidative injury (SOD activity, MDA content, NO level, endothelin concentration) of each group were analyzed. RESULTS: In comparison with model group,the percentage of the lipid plaque area of aortic endothelium and endothelial oxidative injury (except for SOD of VitE group) of SiNi-high and mid-dose group and VitE group are reduced obviously (P