ObjectiveTo study the protective effects of Qiqiong(QQJN) on focal cerebral ischemia/reperfusion injury and its mechanism. MethodsMiddle cerebral artery occlusion(MCAO) was used to make focal cerebral ischemia/reperfusion model by intravascular nylon filament occlusion. The protective effects of QQJN were evaluated by investigating neurological function score, percentage of cerebral infarction, pathomorphology of brain, the activity of SOD and the content of MDA in hrain tissue,thrombogenesis and platelet aggregation in vitro. ResultsCompared with model group, QQJN(4.4、8.8g/kg)could decrease the neurological score in 8 and 22h after reperfusion, reduce the percentage of cerebral infauction,improve pathomorphology of brain, decrease the length, wet weight and dry weight of thromb and inhibit platelet aggregation. ConclusionQQJN had protective effects on focal cerebral ischemia/reperfusion injury. The role of anti-injury of free radicals,inhibit thrombogenesis and platelet aggregation should contribute to its neuroprotective effects.

Aim To study the effects of extract of astragalus on hippocampal delayed neuronal death of totalcerebral ischemia and 7 days reperfusion in rats.Methods Global ischemia was made by four-vessel occlusion. Electron microscope was used to observe the ultramicrostructure of dorsal hippocampal neurons.Light microscope was used to survey the structure of hippocampal neurons and to count the number of normal neurons in CA1 sector. Glial fibrillary acidic protein(GFAP) was detected by immune histochemistry.Results Compared with ischemia and reperfusion group(I/R),EA improved the ultrastructure of hippocampal neurons, suppressed the decrease of normal neurons in CA1 and degraded the expression of GFAP .The number of normal neurons in I/R group was 38?11.5,and in EA(20,40 mg?kg -1) groups,63?12.8(P

Protein-protein interactions and recognition are the focal and hot themes of the life science field in the 21st century. Molecular docking approach is the effective computer modeling technology in the study of this topic. Generally, the protein-protein docking procedure is composed of four stages: searching of the binding modes of the receptor and the ligand, filtering of docked modes to eliminate the irrational docked structures, optimizing the structures, evaluating the docked modes with the refined scoring function and ranking them to obtain the near-native structures. Combining the research group's works, in terms of the international and national progress of protein-protein docking approaches, the detailed review was made about the four stages mentioned above. Additionally, the existing major questions are analyzed and the prospects of the future study are made.

Aim To study the effect of EA on the injury induced by hypoxia/reoxygenation in primary cultures of rat hippocampal neurons.Methods Rat hippocampal neurons in primary culture were used,and a apoptosis model was induced by hypoxia/reoxygenation.MTT assay and LDH releasing rate were used to detect the cell viability.The apoptosis rate of hippocampal neurons was analyzed by Hoechst 33258 staining,flow cytometry with AnnexinV-FITC and PI staining.Western blot was used to detect the protein expression of AKT and p-AKT.Results Compared to control group,three hours of hypoxia followed by sixteen hours of reoxygenation induced hippocampal neuronal apoptosis.EA could raise the neuronal viability and reduce apoptosis rate and the damage degree of rat hippocampal neurons.EA could increase the expressing of p-AKT.Conclusions EA has protective effects on damaged neurons,and the mechanism may be related to activating the PI3K-AKT signal transduction pathway.

Aim To observe the neurological protective effects of astragalosides(AST) on focal cerebral ischemia-reperfusion(I/R) injury in rats and to explore its possible mechanism.Methods Male SD rats received right middle cerebral artery occlusion for 120 min,and were decapitated 1,3,7,and 14 days after reperfusion.AST(40 mg?kg-1) was orally administered after I/R.Neurological deficit score was daily determined,the expressions of BDNF and p75NTR mRNA were detected by RT-PCR,and the expression of TrkB mRNA was detected by real-time PCR.Results AST reduced the neurological deficit score on days 3,increased the expression of BDNF mRNA on days 3,7 and 14,decreased p75NTR mRNA and increased TrkB mRNA on days 3 and 7.Conclusions AST improves the neurological deficits after I/R in rats.The mechanism may be related with increasing BDNF,and TrkB mRNA,and decreasing p75NTR mRNA.

OBJECTIVETo study the protective effects of astragaloside (AST) on memory impairment and the expression levels of amyloid precursor protein (APP) and its mRNA, alpha secretase and beta secretase mRNA in the brain of mice induced by dexamethasone (DEX).

METHODMice were randomly divided into six groups: control group, model group, AST ( 10, 20, 40 mg x kg(-1)) groups and ginsenoside Rg1 (6.5 mg x kg(-1)) group. The animal models of dysmnesy mice were established by intragastrical administration of DEX (5 mg x kg(-1)) for 21 days. Subsequently, the dysmnesy mice were treated by intragastrical administration of ginsenoside Rg1 and different doses of AST (10, 20, 40 mg x kg(-1)), respectively. Morris water maze was applied to evaluate the learning and memory function in mice. The expression of APP, alpha secretase and beta secretase mRNA were analysed by RT-PCR, and immunohistochemistry was used to evaluate the expression levels of APP in cerebral cortex, hippocampus CA1 and CA3.

RESULTAST (20, 40 mg x kg(-1)) could improve the learning and memory function in mice (P<0.05, P<0.01), decrease the expression levels of APP and beta secretase mRNA (P<0.05), increase the expression level of alpha secretase mRNA (P<0.05), and decrease the expression level of APP in cerebral cortex and hippocampus CA1 (P<0.05).

CONCLUSIONAST could improve the learning and memory function in mice, which mechanism may contribtuted to the expression inhibition of APP and APP mRNA, beta secretase mRNA, and promotion of the expression of alpha secretase mRNA.

Amyloid Precursor Protein Secretases ; genetics ; Amyloid beta-Protein Precursor ; genetics ; Animals ; Dexamethasone ; pharmacology ; Male ; Memory Disorders ; drug therapy ; prevention & control ; Mice ; RNA, Messenger ; analysis ; Saponins ; pharmacology ; Triterpenes ; pharmacology

OBJECTIVETo study the effects of Polygona-polysaccharose (PSP) on blood glucose level and the mechanism of protection on diabetic rats induced by streptozotocin (STZ).

METHODThe animal model of diabetes was established by injecting STZ (60 mg x kg(-1)) into its abdominal cavity. The amount of water drinking, food intake, urinary volume and body weight were measured at the fourth week of the treatment. The blood samples were drawn to determine the indexes of blood glucose (FBG) and Glycosylated serum protein (GSP) and blood serum insulin (INS). Pancreatic pathology was studied with morphological method and immunohistochemical method. The distribution of apoptotic cells and the expression of Caspase-3 were observed by TUNEL and immunohistochemistry.

RESULTThe levels of FBG, GSP and the amount of water drinking, food intake, urinary volume in the PSP treated groups were obviously lower than those in the model group while INS increased. PSP decreased the rate of apoptotic cells and the level of Caspase-3.

CONCLUSIONPSP can effectivly decrease blood glucose and increase INS. The mechanism may be related with inhibiting islet cell apoptosis and lowering Caspase-3.

Animals ; Apoptosis ; drug effects ; Blood Glucose ; metabolism ; Blood Proteins ; Caspase 3 ; metabolism ; Diabetes Mellitus, Experimental ; blood ; drug therapy ; metabolism ; pathology ; Disease Models, Animal ; Drugs, Chinese Herbal ; chemistry ; Gene Expression Regulation, Enzymologic ; drug effects ; Glycoproteins ; blood ; Hypoglycemic Agents ; pharmacology ; therapeutic use ; Insulin ; blood ; Male ; Polysaccharides ; pharmacology ; therapeutic use ; Rats

OBJECTIVETo study the protective effects and mechanisms of astragaloside (AST) and astragalus saponin I (ASI) on the memory impairment in senescent rats treated by glucocorticoid (GC).

METHODY maze test was performed to determine the effects of AST and ASI on memory impairment of hydrocortisone(HC)-induced senescent rats. Using Ca2+ sensitive fluorescent indicator (Furo-2), free intracellular calcium concentration ([Ca2+]i) was measured by double wavelength fluorescence sepectrophotometer in thymocytes and hippocampal neurons induced dexamethasone (DEX). And apoptosis was detected by DNA gel electrophoresis and flow cytometry.

RESULTCompared with HC control, AST and ASI can improve the memory of the senescent rats treated by HC, lower [Ca2+]i and suppress apoptosis of thymocytes and hippocampal neurons induced by DEX.

CONCLUSIONAST and ASI can delay the aging in rats treated by HC, and its mechanism may includ lowering[Ca2+]i and suppressing the apoptosis of thymocytes and hippocampal neurons.

Aging ; drug effects ; metabolism ; pathology ; Animals ; Apoptosis ; drug effects ; Body Weight ; drug effects ; Calcium ; metabolism ; Dexamethasone ; adverse effects ; Female ; Glucocorticoids ; adverse effects ; Hippocampus ; pathology ; Intracellular Space ; drug effects ; metabolism ; Male ; Memory Disorders ; chemically induced ; metabolism ; pathology ; prevention & control ; Neurons ; drug effects ; pathology ; Rats ; Saponins ; pharmacology

OBJECTIVETo study the protective effects of Xinaoning freezedrying power (XNN) against global cerebral ischemia-reperfusion injury.

METHODPulsinelli four-vessel occlusion method was used to make global cerebral ischemia-reperfusion model of rats. The EEG and the reappearing time of righting reflex were recorded, and the activity of SOD, LDH, NOS and the content of MDA and LD in the brain were tested. The ET content in hippocampi was researched by radioimmunoassay method. Aggregation of platelets induced by ADP was examined. The resting and free intracellular calcium concentration ([Ca2+]i) in platelets induced by CaCl2 was measured by double wavelength fluorescence sepectrophotometer with a Ca2+ sensitive fluorescent indicator (Furo-2).

RESULTXNN could promote the recovery of EEG and righting reflex, reduce the brain edema and brain index, increase SOD and LDH activities, inhibit NOS activity, decrease MDA, LD and ET contents, inhibit platelet aggregation, reduce the resting [Ca2+]i and inhibit the increase of [Ca2+]i induced by CaCl2 in rats.

CONCLUSIONXNN has protective effect against golobal cerebral ischemai-reperfusion injury.

Animals ; Brain Ischemia ; drug therapy ; metabolism ; Calcium ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Humans ; Male ; Nitric Oxide ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; metabolism