Objective To investigate clinical effect of sIgA combined with Jiawei Yuping Feng pulvis in treatment of upper respiratory infection ( URI) in children.Methods 160 children in hospital diagnosed with URI were randomly divided into treatment group and control group.With basic treatment, the control group were treated with Jiawei Yuping Feng pulvis, twice per day, 3 g each time, orally; treatment group on the basis of control group, secretory IgA via nasal drip, 0.3-0.5 mg/( kg? d) , dividing into 6-8 times.The treatment course was 7 days.The total efficiency, improvement of symptoms and adverse reactions were observed and compared.Results The total effective rate of treatment group (96.25%) was significantly higher than control group (85%)(χ2 =5.96, P<0.05).After 7 days of treatment, WBC and NEUT% of treatment group decreased significantly compared with control group ( P <0.05 ) .The fever, sore throat and runny nose, cough and expectoration symptom remission time of treatment group were significantly shorter than control group (P<0.05).Adverse reactions of both groups were lower.Conclusion It is effective to treat URI in children using sIgA combined with Jiawei Yuping Feng pulvis therapy, and it has few adverse reactions.

AIM: To explore the effects of Angelicae sinensis preparation and sodium ferulate on inflammatory liver injury induced by lipopolysaccharide (LPS) and their molecule mechanism. METHODS: ICR mice were divided into five groups: Angelicae sinensis group, sodium ferulate group, dexamethasone group, inflammation control group and normal group. The model of inflammatory injury in mice was set up by tail vein injection with the bacillus calmette-guerin (BCG) and LPS respectively prior and posterior to administration of those tested drugs. The tested drugs (the preparations of Angelica sinensis, sodium ferulate and dexamethasone) and normal saline were given respectively to the corresponding group. The pathological observation of the liver tissues in mice was made for the intensity of inflammatory liver injuries. The immunohistochemical detection and comparison were performed for the expression of ICAM-1 and E-selectin proteins in the liver tissues in those mice. RESULTS: The intensities of liver inflammatory injuries in mice from drug-treated groups were obviously lighter than that from the inflammation control group (P

AIM: To find out whether traditional Chinese medicine Angelicae Sinensis has direct suppressive effect on schistosome egg-induced granulomatous response. METHODS: The lung model of granuloma response was established by injecting living eggs of Schistosoma japonicum into the tail veins of eggs-sensitized mice then the preparation of Angelicae Sinensis were given intraperitoneally once a day for ten days. In vitro model of granulomatous reaction was set up by incubating dry schistosome eggs together with those splenocytes isolated from schistosome infected-mice or from the mice with pulmonary granuloma formation. Different doses of the preparation was, in the need of experiment, added to culture fluid. The sizes of granulomas formed surrounding single egg in lungs or the intensity of in vitro granulomatous responses were measured and observed. RESULTS: The average diameter of pulmonary granulomas in administered group was significantly smaller than that of the control ( P

Objective To investigate the role of CD4+ CD25+ regulatory T lymphocyte(Tregs)in the immunological pathogenesis of liver fibrosis.Methods Twenty-six rats were divided into two groups:control group(6 rats)and model group(twenty rats).The rat model of liver fibrosis was induced bv subcutaneous injection of carbon tetrachloride(CCl4).The serums were collected for detection of hepatic function and fibrosis parameters.Hepatic tissue samples were used to observe the histopathological changes.The flow cytometry was used to detect the proportions of Tregs in both peripheral blood and spleen.The data were evaluated by t-test.The relationship between two variables was analyzed using Pearson linear correlation.Results The levels of serum alanine aminotransferase (ALT)and aspartate aminotransferase (AST) were significantly increased,but the level of serum albumin (Alb) was obviously decreased.The concentrations of serum hyaluronic acid (HA),procollagen type Ⅲ(PCⅢ),collagen type Ⅳ(CⅣ)of the model group increased to(177.42±61.25)μg/L,(34.86±7.47)μg/L and(7.32±3.71)μg/L,respectively,which were higher than those in the control group(t=-3.670,-5.661,-3.950,respectively;all P<0.01).In model group,hepatic lobules were full of collagen fibers and the hepatic pseudolobule formation was observed.The proportion of peripheral blood Tregs in CD4+ T lymphocyte in liver fibrosis model was(7.41±2.15)%,which was significantly lower than that in control group(12.88±2.93)%(t=3.752,P<0.01).Furthermore,the frequency of Tregs in spleen of the model group was(9.49±1.16)%,which was also significantly lower than that in control group(13.16±2.36)%(t=2.793,P<0.05).In addition,the levels of serum ALT,AST and fibrosis parameters were inverselv correlated with the frequency of Tregs in spleens and peripheral blood(ALT and Tregs in blood:r=-0.727,AST and Tregs in blood:r=-0.698,ALT and Tregs in spleen:r=-0.663,AST and Tregs in spleen:r=-0.535,HA and Tregs in blood:r=-0.719,PCⅢ and Tregs in blood:r=-0.558,CⅣ and Tregs in blood:r=-0.792,HA and Tregs in spleen:,r=-0.424,PCⅢ and Tregs in spleen:r=-0.685,CⅣ and Tregs in spleen:r=-0.506;all P<0.05).However,the linear correlations between serum Alb and Tregs in spleens and peripheral bloods were not observed(r=0.423,0.372,respectively,both P>0.05).Conclusion These findings suggest that the reduction of CD4+ CD25+ Tregs probably play an important role in the immunological pathogenesis of liver fibrosis.

Objective To explore the expression and significance of uncoupling protein (UCP)2in rats models of acute liver failure (ALF). Methods Thirty-six healthy male SD rats were randomly divided into normal control group and model group, and the model group was divided into 5 subgroups:6, 12, 24, 36 and 48 hours sub groups with 6 rats in each sub group. The rat model of ALF was established by intraperitoneal injections of D-galactosamine (D-Gal) and lipopolysaccharide (LPS).Sections of liver tissue were stained with hematoxylin and eosin and observed under optical microscope.UCP2 and UCP2 mRNA in rat liver were determined at different time points with immunohistochemical method and reverse transcription-polymerase chain reaction ( RT-PCR ),respectively. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and malondialdehyde (MDA) concentration in the liver tissues were analyzed at the same time points.Comparisons among all the experimental groups were done by SNK test. Results Infiltration of inflammatory cells and necrosis of hepatic cells were marked in model group,and ALT, AST and MDA in model group were significantly higher than those in control group [(24. 0 ± 2. 0) U/L, (82. 3±16. 9) U/L, (2. 55±0. 22)μmol/g] at all time points. And they reached a peak at 24 h [(8346. 7±1363. 1) U/L, (9766. 7±1274. 1) U/L, (8. 34±1. 13) μmol/g; all P<0. 05]. UCP2 and UCP2 mRNA expressed scarcely in the liver tissues of control group, while increased markedly from 6 to 48 hours after D-Gal/LPS challenge in model group (P<0. 05). They both reached a peak at 24 h. And the discrepancy between consecutive experimental group had statistical significance ( P < 0. 05).Conclusions The rat model of ALF was established successfully by intraperitoneal injections of D-gal and LPS. The expression levels of UCP2 mRNA and UCP2 are consistent with the extent of liver injury and the level of oxidative stress in the rat model of ALF.

Objective To study the protective role of ulinastatin in acute liver failure (ALF) and the effect on the expression of hemeoxygenase-1 (HO-1).Methods Sixty-six S-D rats were divided into three groups:control group,ALF group (model group) and ulinastatin group (intervention group).The rat model of ALF was induced by intraperitoneal injection of D-galactosamine (D-Gal) and lipopolysaccharide (LPS). The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA) were detected dynamically after 6,12,24,36 and 48 h injection.HO-1 mRNA expression in liver tissue was determined by reverse transcriptionpolymerase chain reaction (RT-PCR), and the expression of HO-1 protein was detected by immunohistochemistry.The differences among multiple groups were compared by univariate ANOVA and pairwise comparison was done by least significant difference (LSD). Results D-Gal/LPS injections successfully induced ALF rat model which presented with elevated levels of serum ALT,AST and liver MDA after 6 h injections (F=23.864,38.446,18.051,respectively,all P＜0.01),and peaked at 12-24 h after injections.Twenty-four hours after D-Gal/LPS treatment,the levels of serum ALT,AST and MDA in model group and intervention group were (8 346.7±1 363.1) U/L vs(4 151.3±970.0) U/L,(9 766.7±1.274.1) U/L vs (4 696.7±1 476.9) U/L,(8.34±1.13)μmol/g vs (4.66±0.91 ) μmol/g,respectively,which were significantly higher than those e (24.0±2.0) U/L,(82.3±16.9) U/L,(2.55±0.22) μmol/g,respectively] in control group (F=55.684,55.501,47.843,respectively,all P＜0.01);while those in intervention group were much lower than those in model group (P＜0.01).The expressions of HO-1 mRNA and protein in model group were significantly increased than those in control group (P＜0.01),while those in intervention group were even higher (P＜0.01).Conclusion Ulinastain could up-regulate the expressions of HO-1 mRNA and protein,which indicates that ulinastain may play anti-oxidant and anti-inflammatory roles in ALF through HO-1 pathway.

Objective To investigate the role of recombinant human interleukin 6 (rhlL-6) in calcification and osteogenic transition of cultured human umbilical artery smooth muscle cells (HUASMC), and the possible cell signal transduction way. Methods HUASMCs were isolated by the explant method. HUASMCs were treated with (treatment groups) or without (control group) rhIL-6. Alizarin Red S stain was applied for calcium deposition in extracellular matrix of control ceils and the cells treated with rhIL-6 50 μg/L at day 12. Calcium concentration in cell layer of control group and treatment group (treated with rhIL-6 10 μg/L and 50 μg/L, respectively) was determined calorimetrically by the o-cresolphthalein complexone method at day 3, 6, 9 and 12, and corrected by total cell proteins. The mRNA expressions of bone-specific alkaline phosphatase (BAP), osteopontin (OPN), bone morphogenetic protein-2 (BMP2) and osteoprotegerin (OPG) were estimated by real-time PCR in 12, 24 and 72 hours. OPN, BMP2 and OPG expressions were assessed by Western blotting and the BAP concentration at the same time was checked by fluorometry method . Electrophoretie mobility shift assays (EMSA) was used to detect the binding activity of transcription factor Cbfα1 with or without inhibitors of p38-MAPK (SB203580) and PKC (DHC) after 6 hours stimulation by rhIL-6 10 μg/L. Results rhIL-6 induced a positive Alizarin Red S stain and a time-dose-dependent increasing of cell layer calcium deposition.Compared with control group, rhIL-6 10 μg/L enhanced gene expression and protein levels of BAP and BMP2 at the early time (12 and 24 hours), and of OPN and OPG at later hours (24 and 72 hours). RhIL-6 still induced an increasing of binding activity of Cbfα1, which could be partially blocked by DHC but not SB203580. Conclusions rhIL-6 induces HUASMCs calcification and osteogenie transition in vitro, which may be one of the mechanism involved in IL-6 associated vascular calcification as observed in clinical studies. The role of IL-6 in HUASMCs may partially achieved through the PKC cell signal transduction way.

ObjectiveTo investigate the effects of pravastation intervention on tumor necrosis factor (TNF)-α-indueed ossifie calcification in human umbilical artery smooth muscle cells (hUASMCs). MethodshUASMCs were cultured by tissue explant in vitro, hUASMC were treated with TNF-α 50 μg/L and pravastatin of three different concentrations. The calcium deposition was determined by O-cresolphthalein eomplexone method. The mRNA expression of BAP and OPN was determined by real time-PCR. The protein expression of BAP, OPN and BMP-2 was determined by Western blotting. ResultsPravastatin inhibited the proliferation of hUASMC (r=-0.946, P＜0.01) and decreased the cell calcium deposition (r=-0.973, P＜0.01) in a dosedependent manner. Pravastatin down-regulated the expression of BAP, OPN and BMP-2 induced by TNF-α in a dose-dependent manner (mRNA, r=-0.972, P＜0.01;BAP protein, r=-0.820, P＜0.01;OPN protein, r=-0.972, P＜0.01;BMP-2 protein, r=-0.928, P＜0.01). ConclusionPravastatin can inhibit the proliferation of hUASMC, decrease the cell calcium deposition and inhibit the ossifie calcification of hUASMC induced by TNF-α.

Objective To study the effect of uremic serum on the calcification and osteogenic transition of cultured human umhilical artery smooth muscle cells(HUASMC).Methods Sera from 40 healthy controls(control group),40 nondialysis uremic patients(nondialysis group)and 45 uremic patients on dialysis(dialysis group)were detected fi)r biochemical indexes concerned and used to treat the cultured HUASMC.Alizarin red S stain was applied to examined calcium deposition in the cell layer.Calcium concentration was determined calorimetrically by the Ocresolphtha]ein complexone method,and corrected by total cell proteins.The mRNA expression of bone specific alkaline phosphatase(BAP),osteopontin(OPN)and bone morphogenelic protein 2(BMP2)was estimated by realtime PCR.OPN and BMP2 protein expression was assessed by Western blotting and fluorometry method was used to check the BAP concentration. Results Serum biochemical detection revealed thai both uremic groups had higher levels of phosphate,triglyseride,iPTH,C-reactive protein(CRP)and IL-6,and lower level of fetuin-A than healthy control(P＜0.05).Furthermore,dialysis serum had higher levels of triglyseride,CRP and IL-6 than nondialysis serum(P＜0.05).Compared with control group,both uremic scra induced more cell layer calcium deposition and higher mRNA and protein expression levels of BMP2,BAP and OPN(P＜0.05).Higher mRNA and protein expression levels of above factors were found in dialysis group as compared to nondialysis group(P＜0.05). Conclusions Uremic serum can induce HUASMC calcification and osteogenic transition in vitro,which may be one of the mechanisms involved in vascular calcification of ESRD patients.Microinflammatory state may promote the osteogenic transition and vascular calcification in dialysis patients.

Objective To investigate the dynamic expressions of exchange protein directly activated by cyclic adenosine monophosphate (cAMP) (Epac) in rat model of hepatic fibrosis(HF).Methods Forty-two male SD rats were divided into control group (n = 6) and model group (n = 36)which was divided into six subgroups of day 4, week 1, week 2, week 4,week 6 and week 8 with six rats in each subgroup. The rat model of HF was established by intraperitoneal injection of dimethylnitrosamine (DMN). The pathological changes of liver were observed by Hematoxylin-Eosin and Masson staining. Reverse transcription-polymerase chain reaction (RT-PCR),immunohistochemistry and Western blot were employed to detect the mRNA and protein expressions of Epac1, Epac2 and transforming gronth factor (TGF)β1 during the process of modeling and localization in the liver. The statistical analysis was done using one-factor ANOVA, LSD-t test,Dunnett T3 test and Pearson linear correlation analysis. Results Rat model of liver fibrosis was established successfully. In control group, Epac1 (0. 031 28±0. 008 96) and Epac2 protein (0.034 43±0. 002 45) mainly expressed in the cytoplasm of hepatocytes. In model group, the level of Epac1 decreased at day 4 (0. 023 97±0. 003 81) and week 1 (0. 015 81±0. 002 48) ,then began to increase at week 2 of modeling and peaked at week 6 (0. 039 54±0. 001 43), which had statistical significance compared to the control group (t= 5.47,11.58 and - 6.18, respectively; all P＜0.05). Epac2 protein expression declined after modeling, reached the lowest level at week 4 (0. 011 21 ±0. 001 32), which had statistical significance compared to the control group (t= 24. 50, P＜0. 05). TGFβ1 protein expression increased after modeling and peaked at week 4 (0. 011 30±0.001 03) which had statistical significance (t= -23. 36, P＜0. 05) compared to the control group (0. 002 08 ±0. 000 18). The expressions of Epac1, Epac2 and TGFβ1 mRNA were consistent with the trend of protein levels.Correlation analysis showed that Epac1 protein was positively correlated with the course of HF (r =0. 703, P＜0.01 ), while Epac2 protein was negatively correlated (r = - 0. 409, P＜0.05). Conclusions During the progression of HF, Epac1 expression tends to decrease firstly and increase afterwards,while Epac2 expression declines continually. Epac may be involved in the pathogenesis of HF.