The antagonistic effects of ruthenium red (RuR) on the biological activi-ties of endotoxin (ET) which included the limulus amebocytes lysate test, the local Shw-artzman reaction, decreasing the white blood cell counts, and increase of zinc in periphe-ral blood were observed. The destroyed meshes of endotoxin have been seen under electronmicroscope. The amino-groups of endotoxin increased markedly, which it was treated withRuR. These results indicated that the polycationic residues of RuR may be the effectiveunits of antiendotoxin activity.

The significant changes in morphology and nitric oxide synthase (NOS) activity in cultured human aortic endothelial cells (HAEC) were observed when these cells were exposed to LPS, IL-1? and IFN-?. NOS activity increased at 6h of treatment, the time point that HAEC began to change and elongate. The cell shape became fibroblast like and the length to width ratio of the cells increased 2 times of that of the control at 20h treatment, the time point that NOS activity returned to control level.

Objective: To evaluate the effects and partly mechanism of Qileng decoction(QLD,芪棱汤) resisting focal cerebral ischemia/reperfusion(I/R) injury in rats by apoptosis and signal transduction pathway.Methods: The rats were randomly divided into three groups including sham operation group,normal saline(NS) control group and QLD group.The model of focal cerebral I/R injury was induced by using modified thread embolizing in rats.Rats were evaluated by neurologic function score at 2 hours after ischemia and 2,4,6,12,24 and 48 hours after cerebral reperfusion,and the pathological changes of nerve cells and mitochondria ultrastructure at pallium and hippocampus CA1 region were observed at 24 hours after reperfusion.Immunohistochemical method was performed to examine the expression of cytochrome C(cyt C) and caspase-9 at different time points after reperfusion.Apoptosis of nerve cells in ischemic penumbra(IP) was also characterized by terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling(TUNEL) method.Results: Compared with NS control group,neurologic function scores at different reperfusion time points were improved and the pathological changes were ameliorated at 24 hours after cerebral I/R in QLD group.Mitochondria hydropsia was alleviated,mitochondrial cristae fragmentation and granulum basale shedding were diminished,and mitochondrial basical morphology was retained.Meanwhile,apoptosis index(AI) was decreased and the expressions of cyt C and caspase-9 were reduced in IP in QLD group.Conclusion: QLD intervenes in mitochondria mediated and caspase-9 dependent apoptopic pathway.QLD lowers AI and plays a role of protecting nerve by maintaining mitochondrial basical form,stabilizing mitochondrial membrane and inhibiting the release of cyt C and activation of caspase-9.The above actions are possibly some parts of mechanisms of QLD resisting focal cerebral I/R injury.

AIM: To investigate effects of different therapeutic methods and typical recipes on activation of ERK1/2 in Kupffer cells of rats with fatty liver.METHODS: The rat model of fatty liver was established by feeding high fat diet combinated with distillate spirit.Meanwhile Chinese medicines Shugan fang,Jianpi fang,Huoxue fang,Qushi fang,and Zonghe fang were given to treat different groups respectively.12 weeks later,the Kupffer cells were isolated from livers of control group,model group and different treatment groups by sequential in situ perfusion with collagenaseⅣ and pronase E,density gradient centrifugation,selective adherence.The expression of total ERK1/2 and phospho-ERK1/2 in Kupffer cells of control group,model group and different treatment groups were detected by Western blotting.RESULTS: The expressions of total ERK1/2 and phospho-ERK1/2 were higher in Kupffer cells from model group than those in control group(P