The accumulated evidence indicated atherosclerosis (AS) is associated with a chronic inflammatory reaction. Either by secretion of inflammatory mediator or by modulation of expression of adhesive molecules onvascular surface, vascular endothelial cells play a key role in initiation and amplification of inflammation in artery. The NF ?B transcription factor family is a pleiotropic regulatory of endothelial cells activation and the multiple genes relevant inflammatory cytokines are regulated by NF ?B transcriptional activation in endothelial cells. Selective protection of vascular endothelium and regulation of endothelial inflammation may be rational as the target for anti AS.

OJECTIVE：To explore whether EGb761 could protect against doxorubicin-induced cardiotoxicity, and whether it affects on doxorubicin antitumor activity. METHOD： Doxorubicin-induced rat heart mitochondria damage in vitro and doxorubicin-induced cardiotoxicity in mice were used. The cardiotoxicity were evaluated via spectrophotography, electromicrography and other methods.RESULTS： Doxorubicin markedly induced malondialdehyde formation, adenosine 5′-triphosphatase activity loss, membrane rigidification, swelling, disintegration and lysis of rat heart mitochondria in vitro, all the above pathological and biochemical damages were reduced significantly by EGb761. Cardiotoxicity of doxorubicin in mice as measured by increases of heart Malondialdehyde level and serum creatine phosphokinase activity was significantly alleviated by EGb761. Moreover. The antitumor activity of doxorubicin, as assayed by prolonged life span of mice bearing with H22 hepatoma, was not reduced by EGb761 treatment. CONCLUSION：Ginkgo biloba extract may protect heart against doxorubicin-induced cardiotoxicity without interfering with its antitumor activity in mice.

Liver cell death,including apoptosis and necrosis, is triggered by a number of insults. The apoptotic cascade involving the participation of proteolytic caspases is an important pathway of cell death. Mitochondria play a key role in liver cell death. TNF as an important mediator plays an crucial action in liver cell death. Reactive oxygen metabolites may act directly or through immunological mechanism as initiating factors and modulators in liver cell necrosis and apoptosis. Some intrinsic factors may act on the cascade of liver cell death. The extensive knowledge gained in recent years about the mechanisms of hepatocyte death will lead to new and exciting advances in the prevention and treatment of liver diseases.

Immune mediated liver injury plays a key role in the immunopathogenesis of viral hepatitis and autoimmune hepatitis. The phathogenesis of liver injury involved various kinds of cells including lymphocytes, mononuclear macrophages (Kupffer cells), endothelial cells, stallete cells and liver parenchymal cells. Activation of lymphocytes is the initial step of liver damage, and then that the liver macrophages and NK cells. Crosstalk between these cells expands the damage of liver tissues. Cytokines produced by CD8 + cytotoxic T lymphocytes (CTLs) and CD4 + Th cells and other inflammatory cells lead to the persistent infection and liver injury of patients. To protect hepatocytes against cytopathic effect induced by invalid immune response will provide further insight into the development of new anti hepatitis drugs.

Adhesion molecules are involved in neutrophil-mediated inflammation. Neutropil adhesion to endothelial cell mediated by cell adhesion molecules (CAMs) is the first and critical step during the process of inflammation. Three families of CAMs play a central role in neutrophil-endothe-lial cell interactions : the selectins, the integrins, and the immunoglobulin superfamily. These different types of CAMs interact in a programmed, sequential manner to form neutrophil-endothelial cell adhesion cascade. The initial phase of inflammation, neulrophil slowing and rolling, is mediated by selectins; subsequently, firm adhesion of neu-trophils to vessel endothelial cells occurs via binding of the activated integrins and the endothelial receptors such as intercellular adhesion molecule-1 (ICAM-1); Then, neutrophils transmigrate into the tissues, this process requires chemotactic factors, integrins and PEC AM-1. Because of the important role of CAMs in the process of inflammation. Agents may be used to block the function of CAMs as a strategy of antiinflammatory therapy.

The recent advances in research of oxygen free radicals and its relation to Parkinsons disease (PD) was reviewed. Though there is no exact knowledge of the causes of PD, the role of oxidative stress in the etiology of PD has been focused on. Investigations on patients have shown that PD is under a status of oxidative stress. The biochemical features of dopaminergic neurons in the pathologic site of PD implicate the close relation of oxygen free radicals' generation with the pathogenesis of PD. Besides the oxidative stress hypothesis, other proposed hypotheses are also direct or indirect related to oxidative stress.

Inflammatory response clearly occured in pathologically vulnerable regions of the Alzheimers disease (AD) brain. Many proinflammatory mediators, such as IL-1, IL-6,TNF-? and TGF-?, were significantly up-regulated in the pathophysiological process of AD. In addition to their traditional actions as proinflammatory molecules, AD-specific interactions of the cytokines and amyloid ?(A?) may be pathophysiologically relevant, and there was a reciprocal relationship within the cytokines inducing and being induced by A?.

syuclein is regarded as a presynaptic protein, which may play an important role in neuronal plasticity. However, abnormal accumulation of fibrillar ?-synuclein and mutation of ?-synuclein gene can affect the survival of neurons. Its aggregation and interaction with other proteins are the most critical factors. ?-synuclein is a precursor of non-amyloid component of senile plaques in Alzheimers disease. It is likely that ?-synuclein is associated with Alzheimers pathology. In this paper, we summarize the progress in the normal physical function of ?-synuclein and the mechanism in Alzheimers disease.

Gap junctional intercellular communication (GJIC) has been specu la ted to be a necessary biological function of metazoan cells for the regulation o f growth control, differentiation and apoptosis of normal progenitor cells. Rese arches show that most transformed cells and tumor cells have reduced or abolished GJIC. The prevention of the down regulation of GJIC by the tumor promoters or the restoration of GJIC in neoplastic cells may have potential in prevention and therapy of cancer.

Aim Inflammation is a common characteristic of liver injury induced by hepatitis virus or other factors.The purpose of this paper was to study the modulating effect of bicyclol,a novel anti-hepatitis drug,on related inflammatory molecules.Methods Various non-cytotoxic concentrations of bicyclol were cultured with macrophage RAW264.7 line or mouse peritoneal macrophages for 1 h,and then added adequate lipopolysaccharide(LPS)to activate macrophages.NO and TNF-? levels in the supernatant of the culture medium were determined with Griess reagent and L929 cell bioassay,respectively.The iNOS expression and NF-?B activation were detected by Western blot method.Results Pretreatment of 0.1～0.5 mmol?L-1 bicyclol significantly inhibited NO release and TNF-? secretion from RAW264.7 cell line and mouse peritoneal macrophages induced by 1 mg?L-1 LPS in concentration dependent manners and 0.5 mmol?L-1 bicyclol also down-regulated LPS(1 mg?L-1)-induced iNOS expression and NF-?B activation in the cells.Conclusion Bicyclol has suppressive effect on related inflammatory molecules iNOS expression and NF-?B activation,indicating that bicyclol possesses anti-inflammatory property.