Objective To explore the effects of exogenous glutathione on arsenic distribution and nitric oxide (NO) metabolism in the brain of mice exposed to arsenite through drinking water. Methods Female Kunming mice were randomly divided into 5 groups, eight in each, and the mice were exposed to sodium arsenite through drinking water at doses of 0 mg/L (control) and 50 mg/L arsenic for 4 consecutive weeks, on the fourth week, with the exposure of arsenic, glutathione was given through intraperitoneal injection at doses of 200 mg/kg b.w, 400 mg/kg b.w or 800 mg/kg b.w, respectively for 7 days. In the end of treatment, the samples of blood and brain were collected. Levels of inorganic arsenic (iAs), monomethylarsonic acid (MMA) and dimethylarsenic acid (DMA) were determined by HG-AAS method. Activities of nitric oxide synthase (NOS) and the concentrations of NO were determined with kits. Results Compared with those in single arsenic group, glutathione significantly decreased levels of iAs, MMA and total arsenic levels (TAs) in the blood and levels of DMA and TAs in the brain. Activities of NOS and levels of NO in As group were significantly lower than those in control, however administration of glutathione could ameliorate these toxic effects, and NOS activities in groups treated with 400 mg/kg b.w and 800 mg/kg b.w glutathione were significantly higher than those in single arsenic group. Conclusion Exogenous glutathione may promote methylation of arsenic, therefore reduce arsenic levels in both blood and brain. Moreover, it is proposed that administration of exogenous glutathione can ameliorate the adverse effects of arsenic on NO metabolism in the brain via decreasing the brain arsenic burden.

The result showed that CD3AK induced and expanded in vitro could kill MHC I class - negative K562 (NK - sensitive) and Daudi (NK - resistant) tumor cells in a MHC - nonrestricted manner. Induction of necrosis and / or apoptosis of target cells were responsible for the tumorlytic effect mediated by CD3AK.

A new type of killer cells, named PHA-?CD3LAK, was induced by means of costimulating the peripheral blood mononuclear cells (PBMC) with anti-CD3McAb (?CD3) and rIL-2 after PHA-priming for 48 hours. Some biological characteristics of PHA-?CD3LAK, PHA-LAK and CD3AK were compared. The results showed that PHA-?CD3LAK exhibited some advantages over CD3AK and PHA-LAK in proliferation, cytotoxicity, the expression level of mIL-2R, as well as the utilizing of IL-2, suggesting the synergistic enhancing role of PHA, ?CD3 and IL-2. All three groups of effector cells were heterogeneous populations, predominantly CD3 + CD8 + T cells. The CD8 ~(+) cell percentage of PHA-?CD3LAK was higher than that of the other two groups. The application of PHA-?CD3LAK might open a new prospect to clinical therapeutic approach.

Objective:To study the influnence of elemene or heat shock treatment upon the expression of membrane HSP70 and HSPs genes in HepG 2 cells.Methods:HSP70 expression was observed by immunofluorescence and FCM techniques.HSP70 gene transcription was blocked by ActD.Genechip was used to study the expression of HSPs genes and the genes associated with the control of HSPs transcription.Results:The treatment of either elemene(50 ?g/ml,1 h) or heat shock(42℃,1 h)could increase the membrane expression of HSP70,ActD had a synergistic action with both treatments.HSP70EP(Enhancer Protein) gene was up regulated and HSPA2 gene was down regulated in both treatments.HSF1 gene was up regulated in heat shock treatment but down regulated in elemene treatment.The genes closely correlated with tumor immune,such as HSP70,HSP72,HSP75,HSP90 and gp96 were not changed.Conclusion:Comparing with heat shock treatment,elemene can cause a higher percent of HSP70 membrane expression in HepG 2 cells and that may be caused by its altering the distribution of the already existing HSP70 and/or accelerating the HSP70 mRNA translation.Both treatments can change the expression of genes associated with the transcription control factors of HSPs and decrease HSPA2 gene expression.

BACKGROUND:Liver fibrosis is a kind of chronic and active disease that is caused by various causes and characterized by the excessive accumulation of extracelular matrix. At present, use of Chinese herbs for the treatment of hepatic fibrosis has obvious advantages. Salvia miltiorrhiza has been shown to be highly effective in the treatment of hepatic fibrosis. However, the underlying mechanism needs further investigation. OBJECTIVE:To investigate the effects of TanshinoneⅡA on the expression levels of transforming growth factor-β/Smads signaling pathway related factors transforming growth factor-β, bone morphogenetic protein 7, Smad6 and Smad7 in the liver tissue of rats with hepatic fibrosis. METHODS:SD rats were randomly divided into three groups (n = 10): normal control, model and TanshinoneⅡA-treated groups. Rats in the model and TanshinoneⅡA-treated groups were subtaneously injected with olive oil-diluted 10% CCl4 ( 5 mL/kg) twice a week, 8 weeks in total, to build rat models of hepatic fibrosis. Four weeks after hepatic fibgrosis induction, rats in the TanshinoneⅡA-treated group received subtaneous injection of TanshinoneⅡA til eight weeks. Rats in the normal control group were subcutaneously injected with olive oil. RESULTS AND CONCLUSION: Western blotting and reverse transcription-polymerase chain reaction (RT-PCR) detection showed that in the model group, the expression of transforming growth factor-β in the rat liver tissue was significantly increased (P < 0.01) and the expression of bone morphogenetic protein-7, Smad6 and Smad7 was significantly decreased (P < 0.01) compared with the normal control group. TanshinoneⅡA could obviously reverse the expression of those factors above-mentioned (P < 0.01). The results suggest that TanshinoneⅡA can be used for treatment of hepatic fibrosis by decreasing the expression of transforming growth factor-β and increasing the expression of bone morphogenetic protein-7, Smad6 and Smad7.

Objective:To detect the modulation of the Th1/Th2 bias by the EtOH ext. of roasted perilla seed(RPS) in the anaphylaxis mice model.Methods:The mice were divided randomly into 5 groups, namely 1.28, 0.64 and 0.32 g/kg EtOH ext.of RPS group, anaphylaxis model and normal control. All the mice except for the normal control were sensitized by immunized intraperitoneally on days 0 and 5 with chicken OVA. The cytokine profile including IFN-?, TNF-?, IL-2, IL-4, IL-5 in serum of all the mice were evaluated by FCM.Results:The IFN-?/IL-4 ratio was decreased from 3.93 in the anaphylaxis mice model to 0.87 in the normal control group. The mice in 0.32, 0.64 and 1.28 g/kg EtOH ext of RPS group displayed a down-regulation for serum IL-4 and TNF-? levels and showed increased levels of IFN-? with the correspondent IFN-?/IL-4 ratio of 1.92, 2.85 and 3.14.Conclusion:The EtOH ext. of roasted perilla seed can modulate the Th1/Th2 bias in a dose-dependent manner.

Objective:Normal murine DCs were pulsed with complex of tumor antigen from elemene-combo tumor cell vaccine-heat shock protein 70 of BCG (H TA-HSP70 BCG).Their proliferation and antigen presenting function were evaluated.Methods:The dendritic cells(DCs)were cultured in complete media containing GM-CSF and IL-4 and pulsed with H TA-HSP70 BCG,H TA or HSP70 BCG.Their proliferation and stimulating effects on spleen nonadherent cells were evaluated with MTT assay.Their capability of endocytosing FITC labeled dextran was assayed with FACscan,morphological changes of DC were observed in electron microscope.Results:Proliferation index of DCs pulsed with H TA-HSP70 BCG was 2.107?0.013,proliferation index of DCs pulsed with H TA-HSP70 BCG mixed with normal nonadherent spleen cell was 1.927?0.073.The percent of DCs endocytosed FITC labeled dextran was 58.61%.Above changes were more significant than those of DCs pulsed with H TA or HPS79 BCG.Conclusion:H TA-HPS70 BCG had more potent activity to pulse DC and strengthen antigen presenting of DC.

Objective:To find out the role of JNK/SAPK signaling-transduction pathway in the effect of elemene against hepatocarcinoma, offering the clue to ilustrate the molecular mechanisms of antitumor effects of elemene. Methods: The detection of the distribution of elemene in Hca-F cells was detected by gas chomatography and apoptotic changes in elemene treated. SMMC7721 cells were examined by TEM. After elemene treatment, the activation of JNK/SAPK in HepG2 cellls and the DAXX gene expression in SMMC7721 cells were detected by Western blotting and RT-PCR respectively. Results: Gas chomatography showed that elemene was detected at 8. 42 minute. The SMMMC7721 cells treated by elemene for 3 hours began to show typical apoptotic changes . The JNK/SAPK activity in HepG2 cell treated with heat shock was the highest of all groups and the group treated with elemene was the next and the control group is the lowest one. There was no DAXX gene expression in SMMC7721 cells treated with elemene. Conclusion: Elemene can diffuse into cells. Tumor cell apoptosis treated with elemene may be induced by JNK/SAPK activating and DAXX signal pathway may not play key role in JNK/SAPK activation induced by elemene.

In view of the new situation in rapid variation with food safety and nutrition, and an urgent need of the practical talents in China, this study proposes corresponding reforming measures in improving teaching principle, teaching content, teaching methods, teaching equipment, teaching evalu-ation and training teachers.

BACKGROUND:Some studies have shown that hyperlipidemia can lead to osteoporosis in rats, and exercise can increase the bone mineral density of rats. But the effect of short-time exercise on the bone mineral density of hyperlipdemia induced osteoporosis male rats is unclear yet.
OBJECTIVE:To investigate the effect of short-time middle-load treadmil exercise on the bone mineral density of hyperlipidemia male rats.
METHODS:Twenty-six male Sprague Dawley rats were randomly divided into three groups:control group (n=8), hyperlipidemia group (n=9) and exercise intervention group (n=9). The rats in the control group were fed with normal diet, and the rats in the other two groups were fed with high-fat diet and lasted for 4 weeks to establish the hyperlipidemia models. The rats in the exercise intervention group received treadmil exercise 5 days per week for 4 weeks according to the fol owing schedule:15 m/min for 15 minutes in the 1st week, 15 m/min for 20 minutes in the 2nd week, and then 20 m/min for 20 minutes in the last 2 weeks. Slope grade of the treadmil was adjusted at 0°. At the end of experiment, the rats were sacrificed, and the bone mineral density of the right femur, the morphological change of tibia, the level of plasma alkaline phosphates and calcium content were examined.
RESULTS AND CONCLUSION:Compared with the control group, the distal femur bone mineral density in hyperlipidemia group was significantly decreased (P<0.05);histological analysis of the proximal tibia showed thinning and loss of bony trabeculae arrangement, the gap was widened, and a large amount of fat cel s infiltration or integration into vacuoles in the marrow was observed, the plasma alkaline phosphates was significantly increased (P<0.01). Compared with the hyperlipidemia group, distal femur bone mineral density in the exercise intervention group was increased (P<0.05). After adjust body weight, the whole femur bone mineral density was significantly greater in exercise intervention group compared to hyperlipidemia group (P<0.05). The histological analysis of the proximal tibia showed that the spaces of bone trabeculae decreased and the structure of bone trabeculae compacted, the alkaline phosphates activities were increased (P<0.01). There were no significant differences in serum calcium and phosphates levels between groups. The results show that short-time middle-load treadmil exercise can increase the bone mineral density of hyperlipidemia male rats.