This study was aimed to investigate the effect of Xiao-Jian-Zhong decoction and its disassembled prescriptions on the content determination of paeoniflorin . A gradient HPLC system was used in the quantitative analysis of paeoniflorin on Diamonsil RP-C18 column ( 250 mm × 4 . 6 mm , 5 μm ) with the mixed solvents of acetonitrile and water . The flow rate was 1 . 0 mL?min-1 and the detection wavelength was 230 nm . The results showed that the content of paeoniflorin had great changes comparing with X iao-Jian-Zhong decoction with its different disassembled prescriptions . The analysis of variance showed that the difference among groups was sig-nificant (P < 0.05). SNKq analysis showed that there was significant difference between groups 6 and 1, 6 and 2 , 6 and 5 ( P < 0 . 05 ) . But no significant difference was existed among group 6 , 3 and 4 ( P > 0 . 05 ) . It was concluded that liquorice and cassia twigs were helpful to the dissolution of paeoniflorin in the decoction . But jujube and ginger had few effects . The content of paeoniflorin in group 5 which does not include maltose was the highest among all groups . It may be due to the fact that paeoniflorin was wrapped in the maltose of X iao-Jian-Zhong decoction .

Adult ; Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Biopsy ; Diagnosis, Differential ; Female ; Humans ; Immunohistochemistry ; Lung ; diagnostic imaging ; metabolism ; pathology ; Lung Diseases, Interstitial ; metabolism ; pathology ; Silicosis ; diagnostic imaging ; metabolism ; pathology ; Tomography, X-Ray Computed ; Vimentin ; metabolism

Adult ; Blood Glucose ; metabolism ; Female ; Herbicides ; poisoning ; Humans ; Liver ; physiopathology ; Male ; Middle Aged ; Paraquat ; poisoning

Objective To explore the correlation of Connexion43(Cx43),E-cadherin(E-cad)in breast infiltrating ductal carcinoma tis-sue. Methods The expressions of Cx43 and E-cad proteins were detected in 89 cases breast infiltrating ductal carcinoma tissue,48 cases partition groups. by immunohistochemistry Elivision method. Results The expressions of Cx43 and E-cad has a better consistency in the tumor area,the border area and far cancer area of breast infiltrating ductal carcinoma. For both the negative expression in tumor area same time,the rate of lymph node metastasis was highest. Conclusion Cx43 and E-cad in breast invasive ductal carcinoma has a certain synergy in the process of the occurrence and development,which related to its metastasis occurred.

Idopathic pulmonary fibrosis (IPF),with unknown pathogeny,is a interstitial lung disease. The pathological features are diffuse epithelial-cell lesion and excessive extracellular matrix deposition. Many investigators consider alveolar epithelial cells impairment and abnormal activation,fibroblast proliferation and myofibroblast differentiation as causes,resulting in excessive extracellular matrix disorganization of lung. Recently,it is believed that telomeres and telomerases might play a role in regulating the capacity of fibroblast proliferation and aberrant epithelial repair in IPF. The aim of this article is to review the telomeres,telomerases and their relationship with the idopathic pulmonary fibrosis,furthmore,to identify the etiology and pathogenesis of the idopathic pulmonary fibrosis and provide the study measure for establishing an effective treatment.

OBJECTIVETo evaluate the protective effects of punicosides on alcohol induced acute liver injury in mice and its possible mechanisms as well.

METHODThe 60 mice were randomly divided into normal control, model group, three dose groups of punicosides with low, medium and high, then there is silibinin group. Three dose groups of punicosides and silibinin were given in advance by gavage for 4 weeks, then the mouse model of alcoholic acute liver injury was established. The serum levels of ALT, AST and TG were determined, and the mice were killed to calculate somatic index of liver, thymus as well as spleen. MDA, SOD, GSH-Px and GSH-ST were detected in the liver homogenate. Histopathological changes of the liver were observed by HE staining. The expression of MCP-1 and NF-kappaB in the liver tissues were detected by immunohistochemistry.

RESULTMid and high dose of punicosides reduced the liver index in mice significantly, improved liver steatosis, decreased the level of ALT, AST and TG in serum and the content of MDA in liver homogenate, furthermore the two dose groups increased the activity of SOD, GSH-Px and GSH-ST, inhibited the expression of MCP-1 and NF-kappaB in liver tissue.

CONCLUSIONPunicosides can protect the acute liver damage induced by alcohol.

Alcohols ; adverse effects ; Animals ; Chemical and Drug Induced Liver Injury ; blood ; drug therapy ; metabolism ; pathology ; Chemokine CCL2 ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Gene Expression Regulation ; drug effects ; Liver ; drug effects ; enzymology ; pathology ; Male ; Malondialdehyde ; metabolism ; Mice ; NF-kappa B ; metabolism

Objective To investigate the apoptosis of gastric carcinoma SGC-7901 cell induced by histone deacetylase inhibitor(TSA)and to clarify its mechanisms.Methods The apoptosis-inducing role of TSA on gastric carcinoma SGC-7901 cell was investigated with the help of cell proliferation assay,Annexin V stain,cell flow analyzer and Tunel assay.Western blot,gene chips,real time PCR were employed to study the influence and mechanisms of TSA on the expression of gastric carcinoma cell SGC-7901 p53,bax,etc.Results TSA could induce the apoptosis of gastric carcinoma SGC-7901 cells,increase the expression of p53 and bax,and decrease the expression of bcl-2.survivin and easpase in gastric carcinoma SGC-7901 cells.TSA could transfer AIF and EndoG from mitochondria to nucleus.The apoptosis induced by TSA was brought about through the regulation of multiple apoptosis-related genes,and the apoptosis pathway induced by TSA was caspase-independent.Conclusion TSA can induce caspase-independent apoptosis in gastric carcinoma SGC-7901 cell through the regulation of multiple apoptosis-related genes.

BACKGROUND: Similar to other prosthesis, metal-metal prosthesis would produce plenty of wear particles and metal ions, mainly presented as cobalt (Co~(2+)) and chromium (Cr~(3+)), which can lead to osteolysis, eventually, result in aseptic loosening. OBJECTIVE: To observe the effect of Co~(2+) and Cr~(3+) ions on the cells viability and expression of RANK in rats m0nocyte-macrophage cells (RAW264.7) in vitro. METHODS: Monocyte-macrophage cells (RAW264.7) were cultured in vitro, and then the cells were exposed to Co~(2+) and Cr~(3+) ions. The cell viability was assured by MTT test and the level of RANK Mrna was detected by semi-quantitative RT-PCR at different times. RESULTS AND CONCLUSION: Compared to the control group, MTT test demonstrated that Co~(2+) and Cr~(3+)ions could decrease the cell activity of monocyte-macrophage cells obviously. When the cells were exposed to Co~(2+) Cr~(3+) ions, compared to the control group, the Mrna expression of RANK of the metal ions group was increased at 12 hours (P < 0.05), reached its peak level at 24 hours (P < 0.05), and decreased at 48 hours than that of 24 hours (P < 0.05). The results revealed that metal ions have a cytotoxic effect on monocyte-macrophage cells, stimulate the expression of RANK, and have the potential of facilitating monocyte-macrophages cells transform into osteoclast-like cells.

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

Objective: To observe the effects of nerve block on MA and EA analgesia and mast cells degranulation in adjuvant arthritis rats in order to analyze the difference between the underlying peripheral mechanism of MA and EA analgesia. Methods: Zusanli (ST 36) was chosen as the acupuncturing point on adjuvant arthritis rats. Eighty SD rats were randomized into 10 groups, including control, model, normal+Lido, EA, Lido+EA, DLido+ZEA, Xlido+ZEA, MA, Lido+MA, Dlido+ZMA groups, with 8 rats in each group. Paw Withdraw Latencies and mast cells degranulation ratios were recorded and computed. Results: Compared with model group, the pain threshold (PT) and mast cells degranulation ratios of EA and MA groups were obviously increased (P<0.05 or P<0.01). The analgesia effects of both MA and EA were obviously attenuated after nerve block by pretreated with Lidocaine hydrochloride at the acupuncturing point or at the acupiont of proximal end in the same neural stem while they were not by the same manipulations at the acupoint of distal end. Degranulation ratios of mast cells caused by MA or EA were not obviously affected by nerve block. Conclusion: The effective signal of nerve conduction of MA analgesia is generated after the degranulation of mast cells in the process of acupoints activation or needle sense and it is the direct cause of generation of nerve signal. In the condition of EA, the acupoints activation is caused by the stimulation of electric signal on nerve receptor while the degranulation of mast cells is concomitant or feedback effect.