Objective To investigate the effect of Astragalus Membranaceus( Ast) and Angelica Sinensis( Ang) on antithrombosis and explore the molecular mechanism. Methods Plasminogen activator inhibitor-1 ( PAI-1) expression and activity were selected to observe the antithrombosis effect of Ast and Ang ( 3 and 6 mg/ml) on 0. 5 ng/ml TGF-?1 treated endothelial cells. PAI-1mRNA expression was detected by RT-PCR,PAI-1 antigen assay was detected by specific enzyme-linked immunosorbent assays( ELISA) ,and PAI-1 activity was measured by amidolytical assay. Results Ast and Ang significantly inhibited PAI-1 mRNA expreesion,antigen and activity in endothelial cells. The more powerful effects could be observed when treated by Ast and Ang together. Conclusion The PAI-1 mRNA expression,antigen and activity is inhibited effectively by Ast and Ang,which may be the mechanism of their treatment for antithrombosis.

Aim To study molecular mechanisms of the effects of paeoniflorin on increasing expression of erythropoietin.Method RT-PCR and Western blot were used the investigate the influences of paeoniflorin,PI-3 kinase inhibitor (LY294002 30 ?mol?L-1),antagonist of adenosine A1 receptors(DPCPX 10 ?mol?L-1),agonist of A1 receptors(CPA 1 ?mol?L-1) and antagonist of adenosine A2a receptors(SCH58261 0.2 ?mol?L-1) on expression of erythropoietin in hypoxia and normoxia.Results Paeoniflorin decreases the expressions of erythropoietin in normoxia.However, paeoniflorin(2 ?mol?L-1) significantly increases the expression of erythropoietin mRNA after exposure to hypoxia environment from 8 to 24 hours in HepG2 cells.And this phenomenon is inhibited by LY294002,DPCPX and SCH58261.Conclusion Paeoniflorin increases erythropoietin mRNA levels by activating PI-3 kinase pathway through adenosine A1 and A2a receptors.

Many kinds of pathological irritations often make local-tissue face environmental hypoxia.These changes were messaged by increased accumulation of extracellular adenosine through their receptors.There are different roles for the four subtypes of adenosine receptors designated A1、A2a、A2b andA3.This review covers the effects of adenosine A1 receptors in different systems,such as protective effects on cells,improving immune response,regulation of blood pressure and glucose homeostasis.

OBJCTIVE To investigate the protective effect of ferulic acid (FA) on lipopolysaccharide (LPS)-induced damage to PC12 cells and hippocampal neurons in Sprague-Dawley (SD) rats and its potential mechanisms. METHODS ① in vitro study:PC12 cells were pretreated with FA 2.5-40 μmol · L-1 for 12 h and treated with LPS for another 8 h. CCK-8 kit was used to test PC12 cell viability. Inflammatory cytokines tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)were de?tected by ELISA kits. Laser scanning confocal microscopy was performed to measure F-actin expres?sion in the cells. ②in vivo study:FA 25,50 and 100 mg · kg-1 was ip given to Sprague-Dawley(SD) rats once a day for 35 d,and from the 29th day,ip co-administered with LPS(0.2 mg · kg-1)for 7 d. Immunohistochemistry method was used to determine protein expression of phophodiestera 4B (PDE4B)in the hippocampus of rats. The protein expression of cAMP response element-binding protein (CREB) and phospho CREB (p-CREB) was determined by Western blotting. RESULTS In the in vitro study,compared with LPS group,cell viability was significantly increased in FA 10,20 and 40μmol·L-1 groups(P<0.05),while the production of inflammatory cytokines TNF-α and IL-1β decreased(P<0.05). The structure and distribution of cytoskeletal protein F-actin were ameliorated markedly in PC12 cells. In the in vivo study,hematoxylin-eosin(HE)staining showed that pretreatment with FA(50 and 100 mg·kg-1) alleviated the damage to the hippocampus induced by LPS in SD rats. Immunohistochemistry showed that FA(50 and 100 mg·kg-1)pretreatment effectively prevented LPS-induced up-regulation of PDE4B expression in the hippocampus of rats(P<0.05). Western blotting analysis showed that the inhibitory effects on the protein expressions of CREB and p-CREB induced by LPS were altered by FA(50 and 100 mg · kg-1)pretreatment(P<0.05). CONCLUSION FA can protect against LPS induced damage to PC12 cells and hippocampal neurons of rats. The resistant effect on neuron-inflammation of FA may be conferred by inhibiting LPS-induced up-regulation of PDE4B and stimulating signaling pathways of cAMP/CREB.

Objective To investigate the relationship between serum prealbumin (PA) and inflammation in acute myocardial infarction (AMI) patients. Methods A prospective observational study was conducted. AMI patients hospitalized in the cardiovascular department of the General Hospital of Chinese People's Armed Police Forces from June 2014 to June 2016 were enrolled in the study. At the same time, healthy cases were enrolled as control. Venous blood was taken from patients at admission. Serum PA was detected by immune projection turbidimetry method and high-sensitivity C-reactive protein (hs-CRP) was measured by latex enhanced immune turbidimetry. High-sensitivity cardiac troponin T (hs-cTnT), and interleukin (IL-6, IL-8) was measured by electrochemical luminescence method. Creatine kinase-MB isoenzyme (CK-MB) was detected by rate method. PA, inflammatory factor and myocardial enzyme were compared between two groups. The correlation between PA and inflammatory factors was analyzed by Pearson linear correlation; The diagnostic value of PA was analyzed by receiver operating characteristic (ROC) curve. Results 173 AMI patients and 86 healthy controls were enrolled in the study. There were no significant differences in gender, age, history of smoking, hypertension and diabetes. Compared with the control, the levels of serum PA in AMI patients was lower [PA (g/L): 0.215±0.056 vs. 0.280±0.057], hs-CRP, IL-6, IL-8, hs-cTnT and CK-MB were higher [hs-CRP (mg/L): 6.63±3.52 vs. 2.25±1.45, IL-6 (ng/L): 38.03±22.43 vs. 6.13±3.38, IL-8 (ng/L): 295.61±98.70 vs. 17.24±7.31, hs-cTnT (μg/L): 4.789±2.874 vs. 0.009±0.008, CK-MB (U/L): 244.48±165.54 vs. 12.20±5.24], the difference was statistical significant (all P < 0.01). It was shown by Pearson correlation analysis that the levels of PA were negatively related to hs-CRP, IL-6 and IL-8 (r = -0.562, -0.591, -0.548, all P <0.05). The PA level had no correlation with hs-cTnT and CK-MB (r = -0.018, -0.149, both P > 0.05). It was shown by ROC curve analysis that area under ROC curve (AUC) of PA for diagnosis of AMI was 0.783±0.039, and the 95% confidence interval (95%CI) was 0.706-0.860 (P < 0.05). When the cut-off value was 0.190 g/L, the sensitivity was 29.63%, and the specificity was 62.22%. Conclusion PA may be involved in the inflammatory process of AMI and had a diagnostic value for AMI.

Aim To evaluate the effects of ferulic acid ( FA ) on lipopolysaccharide ( LPS )-induced neuroin-flammation in microglia cells and its potential mecha-nisms. Methods Microglial activation was induced by stimulation with LPS, and the effects of FA pretreat-ment on microglial activation and production of proin-flammatory mediators, nitric oxide/iNOS were investi-gated. The role of the mitogen-activated protein kinases in the antiinflammatory actions of FA in LPS-stimulated microglia was further elucidated. Results Cell viabil-ity experiments revealed that FA did not produce cyto-toxicity in microglia. FA significantly inhibited LPS-in-duced production of tumour necrosis factor-alpha ( TNF-α) , interleukin-6 ( IL-6 ) , interleukin-1 beta ( IL-1β) , and nitric oxide ( NO ) . Protein and mRNA levels of COX-2 and inducible nitric oxide synthase ( iNOS) were also attenuated by FA. Further experi-ments on intracellular signalling mechanisms showed that inhibition of extracellular regulated kinase ( ERK) contributed to the anti-neuroinflammatory actions of FA. Conclusion The results suggest that FA inhibits LPS-induced microglial inflammation by partial targe-ting of ERK signalling and attenuation of ERK.

Hypnotic is the choice drug which etiologically and semeiologically treats insomnia. One of the key points for the hypnotic study is to design and choose satisfactory animal models, which links the preclinical foundation research to the clinical research. In this paper, according to the different models building theories——Traditional Chinese Medicine and modern medicine, the mechanisms, methods, advantages and disadvantages, applicable conditions of the insomnia animal models building were reviewed briefly.

Aim To evaluate the effect of CYP1A1 on intracellular Ca2+ in human vascular endothelial cells(HVEC304).Methods The expression plasmid of human CYP1A1 was constructed,HVEC304 was transfected,and the intracellular calcium ion level was monitored by microfluorescent technique.Result The expression plasmid of human CYP1A1 was constructed and its expression location was extranuclear.In HVEC304 cells over-expressing CYP1A1(HVEC304-CYP1A1),Ca2+ basal level decreased obviously(P

Radiation-induced skin injury refers to the acute and chronic skin damage caused when skin is exposed to radiation. Radiation-induced skin damage may be created by nuclear disaster, radiation accident, radiation therapy, occupational exposure and so on. Approximately 95% of patients receiving radiotherapy will eventually develop into radiation-induced dermatitis during or after the treatment. As a consequence, how to appropriately prevent and remedy radiation-induced skin injury is of great practical significance. According to traditional Chinese medicine, radiation-induced skin injury belongs to fire, heat and toxin, blocking Qi and blood, injuring the muscle surface, affecting the distribution of Qi, blood and body fluid in the body, and damaging the function of viscera. This paper summarizes the cognition and development of traditional Chinese medicine theory of radiation-induced skin injury, as well as the research progress of internal and external treatment of traditional Chinese medicine, so as to provide a basis for the research and treatment of radiation-induced skin injury with traditional Chinese medicine.

Objective E0703 is derived from estradiol and has anti-radiation effects on irradiated mice, the effects of E0703 on cell viability,cell cycle and the related mechanism in irradiated AHH-1 cells were investigated in this study.Methods Cell viability,cell apoptosis and cell cycle were determined by Cell Counting Kit-8.Annexin V-FITC double staining kit and Flow Cytometry,respectively.Level of mRNA and protein were detected by RT-PCR and Western blot,respectively.Results 3.0 Gy 60 Co γ-rays induced significant cell cycle arrest,necrosis,apoptosis and reduction of viability.Pretreatment with E0703 for 12 h before irradiation could increase cell viability and regulate cell cycle.but had no obvious effect on cell necrosis and apoptosis.The expression of cell cycle arrest related molecules Rb and MDM2 were increased after 3.0 Gy irradiation,but decreased significantly with pretreatment of E0703.Moreover.the phosphorylation of Rb was also increased.Conclusions The radioprotective function of E0703 might be exerted through influencing on cell cycle and promoting cell proliferation instead of apoptosis or necrosis.