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.

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.

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.

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 investigate the changes of cardiac function, oxidative stress and apoptosis in myocardium of rat model of heart failure induced by adriamycin (ADR). METHODS: At the end of the study, we observed content of malondialdehyde (MDA), activity of superoxide dismutase (SOD) and apoptosis. Expression of P53 protein and p53 mRNA were measured with immunohistochemical method and RT-PCR, respectively. RESULTS: Our data showed that content of MDA increased, activity of SOD decreased and apoptosis in myocardium happened while cardiac function decreased after ADR treatment. p53 gene expression and P53 protein obviously increased in heart failure group. CONCLUSION: There were oxidative stress and apoptosis occurred significantly in a model of heart failure induced by ADR. p53 gene might play an important role in the apoptosis. Correlation analyses suggested that apoptosis in myocardium is related to oxidative stress in ADR-induced heart failure.