OBJECTIVE: To investigate the effect of ultrasonic extraction in the determination of Chanfukang gran- ules. METHODS: Different types of ultrasonic extractor were used to determine the same sample repeatedly .RESULTS & CONCLUSION: The extraction effects were different in using ultrasonic extractors with different power levels and ultrasonic frequency.

Mitochondrial dysfunction has been implicated in the aetiology of sporadic Parkinson's disease but its role in the disease mechanism remains unclear.To investigate the effect of synuclein on mitochondrial dysfunction induced by rotenone.The human dopaminergic SH-SY5Y cells were used as a cell model.The cells over-expressed the wild-type ?-synuclein were treated with complex I inhibitor rotenone.The cell viability,complex I activity,Mitochondrial swelling and O2-content were tested at different time point-1w,2w,4w after rotenone treated.CCK-8 test results showed that the cell viability of overexpressed ?-synuclein(SH-SY5Y-Syn)was much lower than the control group(SH-SY5Y-Ctr).After administrating with rotenone about 1w or 2w the cell viability of SH-SY5Y-Syn became higher than that of SH-SY5Y-Ctr.On the 4th week the results were contrary to the first 2 weeks.Similar results were got when test the mitochondrial function.In the first 2 weeks after roteoone administrating,the mitochondrial function of SH-SY5Y-Syn was better than that of SH-SY5Y-Ctr.This suggest that the ?-synuclein could protect the mitochondrial against the injury induced by rotenone in the early stage-1w,2w,while this effect disappeared in the final stage-4w.

The nuclear factor erythroid 2 related factor 2 (Nrf2) is a key protein of endogenous antioxidant defense systems in the body. In response to oxidative stress, Nrf2 translocates to nucleus and binds to antioxidant response elements (ARE), regulating the expression of a large amounts of antioxidant genes and maintaining a proper redox balance. The pathological processes of neurodegenerative diseases are associated with generation of reactive oxygen species, which cause oxidative stress. Oxidative stress plays a cardinal role in the onset and progression of neurodegenerative diseases. Nrf2-inducer compounds can reduce oxidant stress and have shown therapeutic efficacy in many neurodegenerative disease models. How to activate the Nrf2 signaling pathway effectively has been received much attention. Here we provided an overview of specific mechanism of Nrf2-ARE pathway and the protective effects of Nrf2 in different neurodegenerative diseases, and summarized the Nrf2 activators recently in preclinical study.
Antioxidants ; physiology ; Humans ; NF-E2-Related Factor 2 ; physiology ; Neurodegenerative Diseases ; metabolism ; Oxidative Stress ; Reactive Oxygen Species ; metabolism ; Signal Transduction

Objective To observe the role of dual-source CT (DSCT) in the diagnosis of coronary artery fistula. Methods Nine patients with coronary artery fistula were examined with dual-source CT coronary artery angiography. Then the source images were post processed using volume rendering (VR), multiple planar reformation (MPR), maximum intensity projection (MIP) and curved planar reformation (CPR), and sequential segmental analysis of the intracardiac and extracardiac anomalies was performed. Results Coronary artery fistula in all the 9 patients were accurately displayed with DSCT, including 2 with left main trunk to right ventricle fistula, 7 with left main trunk and (or) left anterior descending artery to main pulmonary trunk fistula, 5 with complex coronary-pulmonary artery fistula. Conclusion Dual-source CT coronary artery angiography is convenient, fast, non-invasive, and may be the preferable method for diagnosis of coronary artery fistula.

Objective To investigate the effects of hyperbaric oxygenation(HBO)therapy on serum con- centrations of soluble intercellular adhesion molecule-1(slCAM-1),soluble vascular cell adhesion molecule-1(sV- CAM-1),soluble E-selectin(sE-selectin)and matrix metalloproteinase-9(MMP-9)in patients with aeute cerebral infarction and their clinical implications.Methods One hundred and twelve cases of cerehral infarction in the ca- rotid artery system were assigned into two groups.Patients in the routine treatment group(RT group,n=62)were treated with routine clinical treatment regime,whereas those in the HBO group(n=50)were treated with H BO ther- apy in additioo to routine clinical treatment.Thirty age- and sex-matched normal subjects were recruited and served as controls.The serum concentrations of sICAM-1,sVCAM-1,sE-selectin and MMP-9 were measured hy using ELISA method before and 10 days after treatment.The assessment of neurological deficits using National Institutes of Health Stroke Scale(NIHSS)score was conducted before treatment,and at 10 and 30 days after treatment,and the therapeutic efficacy was evaluated.Results The concentrations of sICAM-1,sVCAM-1,sE-selectin and MMP-9 of the patients were significantly higher than those of the control subjects.These parameters were all decreased signifi- cantly after treatment in the two patient groups.Moreover,these parameters were lower in the HBO group than those in the RT group after treatment.The NIHSS scores of HBO group were significantly lower than that of the RT group at the 30th clay post-treatment.The effective rate of HBO group was higher than that of RT group.Conclusion HBO therapy can decrease the serum levels of sICAM-1,sVCAM-1,sE-seleetin and MMP-9,which might be one of the mechanisms of HBO in the treatment of cerebral infarction.

Carotenoids play an important role in regulating the hydrogen production of hydrogen-producing Rhodobacter sp. The carotenoids of hydrogen-producing Rhodobacter sp. grown in acetate medium were extracted by using acetone-methanol (7∶2,V/V) solvent and were separated by using thin-layer chromatography on silica-gel plate. The qualitative and quantitative of the carotenoids were analyzed by spectrometry. The results showed that the carotenoids were completely extracted three times with acetone-methanol (7∶2,V/V) in two hours. The ultrasonication had little effect on yield of carotenoids. The yield of carotenoids was 2.81mg/g wet cell. There were 4 spots on the silica-gel plate in the order of yellow, red, light red and light yellow. Yellow spot and red spot were the dominant composition of carotenoid in Rhodobacter sp. The spectrometry data showed that the yellow and red component might be the spheroidene and spirilloanthin respectively.

Objective To investigate the inhibitory effect of paclitaxel on rat graft arteriosclero- sis and the mechanism.Methods The rat abdominal aortic allograft model was used.All rats were divided into three groups:isograft control group (Wistar to Wistar),allograft group (Wistar to SD) and allograft paclitaxel-treated group (Wistar to SD).Rats in allograft paclitaxel-treated group re- ceived paclitaxel (2 mg?kg~(-1)?d~(-1)) from the operation day to post-operative day 14 and others received same dosage of vehicle (0.9% normal saline).Animals were sacrificed and the grafts were harvested at 30th day after operation.Intimal proliferation was studied by light microscopy.The apoptosis of vascular smooth muscle cells (VSMCs) was detected by transmission electronic microscopy and termi- nal deoxynucleotidyl transferase biotin nick end-labeling (TUNEL) method.Results Morphological analysis showed that grafts had no change after operation in isograft control group,but in allograft group intimal proliferation,inflammatory cells infiltration in neointima and adventitia and stenosis of allografts were obvious.After treatment with paclitaxel,there was a significant decrease in intimal proliferation,inflammatory cells infiltration and stenosis.Apoptosis index of VSMCs was higher in the allograft paclitaxel-treated group than other groups.Conclusion Paclitaxel can inhibit intimal pro- liferation in aortic allografts and prevent the graft from arteriosclerosis possibly by inducing the apoptosis of VSMCs.

Objective To investigate the distribution of neurons expressing Fos protein in central nervous system (CNS) following esophageal mucosal acid exposure,and to map the contribution of spe- cific brain areas in sensitizing responsivity and emphasize the coding change of CNS to the esophageal acid stimulation.Methods Thirty-six healthy Sprague-Dwley rats were randomly divided into five groups. Group A (n=6) was normal group of home cage control animals to which no stimulation was given. Group B (n=7) was saline group which received esophageal perfusion with normal saline solution (0.9% NaCl).Group C (n=8) was treated with esophageal mucosal acid exposure containing 0.1 mol/L HCl. Group D (n=7) was sensitized by ovalbumin.Group E (n=8) received basal ovalbumin-sensitization plus esophageal mucosal acid exposure.The rat model of esophageal visceral hypersensitivity was estab- lished by the basic ovalbumin-sensitization combined with intra-esophageal mucosal acid exposure.The neuronal expressions of c-fos proto-oncogene were detected with immunohistochemical counter-staining and computerized color image analyzer under various conditions.Results The rats in model group with basic ovalbumin-sensitization plus esophageal acid perfusion initiated a high density expression of c-fos- immunoreactive(Fos-IR) neurons in multineuronal networks.A significantly higher number of Fos positive neurons was found in the model group than those in the corresponding regions of other groups (P＜0.05) in the following brain areas:frontal and parietal cortex,insular cortex,cingulated cortex,central amyg- daloid nucleus,the K(?)lliker-Fuse nucleus,the nucleus ambiguus,parabrachial nucleus,hypothalamic paraventricular nucleus,paraventricular thalamic nucleus,paratrigeminal nucleus,the nucleus of solitary tract,area postrema,reticular nucleus of medulla,whereas no significant difference was found in the dorsal motor nucleus of the vagus,supraoptic nucleus,periaqueductal gray matter or orbital part of infe- rior frontal gyrus.The values of Fos-IR neurons were also increased in the central amygdala,parabrachi- al nucleus,paraventricular nucleus,the paratrigeminal nucleus and NTS in the model group than that in the corresponding regions of other groups (P＜0.05).Conclusion The basic ovalbumin-sensitization fa- cilitated dramatically the c-fos expression evoked by esophageal acid perfusion,suggesting that visceral hypersensitivity induced by ovalbumin may alter cortical reactivity processing of esophageal acid stimula- tion in brain areas.

Objective:To identify the effect of ?-synuclein overexpression on mitochondrial membrane structure with atomic force microscopy. Methods:?-syn expression was mediated by AAV (adeno-associated viral vector) and Recombinant AAV/?-syn and AAV/LacZ viral particles were stereotaxically injected in the left side of rat substantia nigra (SN) for rat model of ?-synuclein overexpression. Mitochondria were isolated from rats SN of Brain. Mitochondria were analysis with JC-1 staining,atomic force microscopy and Western blot. Results:By 16 weeks post-infection of AAV-?-syn,the level of ?-syn increased about 2 times in mitochondrial fraction with Western blot and mitochondrial membrane potential (??) decreased with JC-1 staining. Furthermore,mitochondria swelling and porous like structure formed on the mitochondrial membrane with atomic force microscopy. Conclusion:The data suggested that ?-syn could accumulate in mitochondria,might form mitochondrial membrane pores and lead to ?? decreases. ?-syn might lead to mitochondrial dysfunction in Parkinson's disease.

Objective: To identify the functional domain of ?-Synuclein in affecting mitochondrial function and how the function to be impaired,especially,the mitochondrial membrane potential and the release of Cytochrome c.Methods: Harvest of ?-Syn-N and ?-Syn-△N by PCR,then subcloned into the pCMV-Myc mammalian expression vector.The recombinant plasmids were transfected into HEK293T cells by Lipofectamine 2000.After detecting the protein expression by Western blot,the functional domain was detected by co-immunoprecipitation.The mitochondrial membrane potential through flow cytometry and immunofluorescence,at the same time,the release of Cytochrome c through flow cytometry to detect.Results: The recombinant plasmids were constructed successfully.CO-IP has proved that N-terminal may be the functional domain of ?-Synuclein in affecting mitochondria.Over-expression of N-terminal could depolarize the mitochondrial membrane potential and induce the Cytochrome c releasing in MN9D cells.Conclusion: N-terminal may be the functional domain of ?-synuclein and over-expression of N-terminal could decrease mitochondrial activity.