AIM: To determine the dissolution of Longdan Xiegan Pills(Radix et Rhizoma Gentianae,Radix Scutellariae,Fructus Gardeniae,etc.) on the basis of markers such as gentiopicroside,baicalin and geniposide. METHODS: According to Appendix ⅩCⅢ of Chinese Pharmacopoeia 2005 edition VolⅡ,dissolution medium was 100 mL 0.5% SDS aqueous solution and rotating speed was 100 r/min.The dissolution solution of pill was taken and analyzed by HPLC method.A column of Kromasil C_(18)(4.6 mm?250 mm,5 ?m) was used.The mobile phase composed of A acetonitrile,B 1% glacial acetic acid aqueous solution,gradient eluation.The flow rate was 1.0 mL/min with the detection wavelength at 254 nm. RESULTS: The average dissolution of three batches of gentiopicroside,baicalin and geniposide exceeded the marker amount by factor of 0.75 time in 4 h. CONCLUSION: A reliable and qualitative method is established with good reproducibility for determination of dissolution of Longdan Xiegan Pills.

After the application of RFID in domestic libraries, its outcomes and related problems were described, the authors pointed out that Internet of Things-based smart library is the future library direction.

AIM: To study the effect of high fat diet on the expression of sterol regulatory element biding protein-1 (SREBP-1) and transforming growth factor β_1 (TGF-β_1) in renal tubular cells and rosiglitazone intervention. METHODS: Wistar rats were treated with high fat diet and rosiglitazone for 3 months. The serum glucose, serum insulin and serum triglyceride were detected. Oil Red O staining was used to observe the renal lipid deposit and Masson staining was for the detection of ECM accumulation. SREBP-1, TGF-β_1 and FN protein were determined by the methods of immunohistochemistry and Western blotting. SREBP-1 mRNA was detected by in situ hybridization. RESULTS: Rosiglitazone prevented effectively the increase in serum glucose, serum insulin and serum triglyceride resulted from high fat diet. High fat diet led to lipid droplet formation in renal tubular cells and interstitial ECM accumulation, which was decreased by rosiglitazone treatment. Compared to normal rats, SREBP-1 protein and SREBP-1 mRNA showed high expressions in high fat diet rats that were lowered by rosiglitazone. The precursor segment and mature segment of SREBP-1 protein were decreased by 27.39% and 27.32%. Similarly, the high expressions of TGF-β_1 and FN protein in kidney of high fat diet rats were also prevented by rosiglitazone intervention. Compared to high fat diet rats, the expression of TGF-β_1 in rosiglitazone treatment rats was lowered by 19.14%. CONCLUSION: Rosiglitazone prevents effectively the over-expression of SREBP-1 and TGF-β_1 in renal tubular cells, and decreases lipid accumulation and ECM production in rats fed with high fat diet.

significantly increased (all P < 0.01). Following SREBP-1 was down-regulated by siRNA, high glucose-stimulated TGF-β1 and FN protein expressions were decreased by 17.9% and 24.6% ,respectively(all P<0.01).

Objective To investigate the protective effects and mechanism of Pentoxifylline(PTX) on rats with renal interstitial fibrosis following unilateral ureteral obstruction(UUO).Methods The rats were randomly divided into 5 groups: Sham operation group(group A),UUO group(group B),Enalapril group(group C),PTX group(group D) and PTX plus Enalapril group(group E).On the 3th,7th and 14th day after operation,5 rats of each group were sacrificed by exsanguinations,respectively.The concentration of hydroxyproline was measured,and the ratio of collagen and renal weight was tested.The expressions of transforming growth factor-?1(TGF-?1),tissue inhibitor of metalloproteinase-1(TIMP-1),vascular endothelial growth factor(VEGF),bone morphogenetic protein-7(BMP-7),NF-?B and CD34 were measured by immunohistochemistry.The peritubular capillary index(PCI) was regarded as the expression of CD34.Results The ratio of collagen and renal weight in the rats of group B was higher than that of other 4 groups(P

Objective To study the relationship between lung ventilation function of workers exposed to rare earth dust and their IL-2,IL-6 and TNF-α gene polymorphism.Methods TNF-α gene polymorphism were identified by RFLP-PCR,IL-2 and IL-6 gene polymorphisms were identified by PCR-CTPP analysis.Lung ventilation function was deteced by instrument of ventilation function.Results Compared with controls,there was no statistic significance in frequencies distribution of TNF-α gene polymorphism(X2=4.03,P＞0.05),IL-2 gene polymorphism(X2=2.21,P＞0.05)and IL-6 gene polymorphism(X2=1.05,P＞0.05).Compared with IL-2 gene wild type,IL-2 homozygote type increased the risk of lung ventilation dysfunction by 4.29 folds(95% CI 1.09～16.9).Conclusions Compared with controls,incidence of ventilation function of workers exposed to rare earth dust is in ascending trend.IL-2(G/G)gene type induces more serious inflammation reaction than the others.

Aim To investigate the regulatory effect of p38MAPK signal pathway on the apoptosis of human esophageal cancer cells induced by valdecoxib.Methods The tumor cells were inoculated in the dose of 1?107?L-1.After 6 h,the cells were divided into control group,solution group,400,200,100,50,25 ?mol?L-1 valdecoxib group and various concentration valdecoxib+SB203580 group,cultured for 72 h.FCM and DNA Ladder were used to detect the apoptosis of Eca109 cells.p38 mRNA expression was detected by RT-PCR.The expression of p-p38MAPK protein was detected by immunohistochemical staining and FCM.Results ① Valdecoxib could increased the apoptosis rate of Eca109 cell in concentration-dependent fashion.Apoptosis rate was increased to 48.46% in 400 ?mol?L-1 valdecoxib group at the incubation time of 72 h.DNA ladder was the most recognized marker of apoptosis,and there was obvious DNA ladder in valdecoxib treated group,especially in 400 ?mol?L-1 group.② Valdecoxib could increase the expression of p38MAPK,while SB203580 could inhibit the over-expression induced by valdecoxib,at the same time,the apoptosis rate was been decreased.③ The expression of p38MAPK protein was positively correlated with the apoptotic rate(r=0.822,P=0.000).Conclusions Valdecoxib could activate p38MAPK pathway,thus induce the apoptosis of Eca109 cells,which may be one of the mechanisms for the inhibition of cell growth by valdecoxib.

Aim To investigate the effects and possible mechanism of valdecoxib on apoptosis of cancer in nude mice.Methods The tumor model was established by inoculating 2?106 cell both in the left and right armpit respectively.The mice were divided randomly into control group and valdecoxib group(20 mg?kg-1?day-1).Valdecoxib was dissolved in carboxymethylcellulose sodium and administered from the second day after inoculation.The mice were killed after 4 weeks.The volumn and inhibitory rate were calculated according to the length and width of xenograft tumor.H.E staining was used to observe the cell structure of the stomach and colon.The apoptotic rate was detected by FCM.The expression of COX-2,c-jun and c-fos protein was detected by FCM and immunohistochemical staining.Total RNA was extracted with Trizol method and the expression of COX-2 mRNA was detected by RT-PCR.Results(1) The body weight of nude mice was higher in valdecoxib treated group in a time-dependent manner.(2) Valdecoxib inhibited the growth of tumor.The weight of tumor was decreased from(1.43?0.52)g in control group to(0.93?0.53)g in valdecoxib treated group.The ratio of inhibition on the growth of tumor was 45.80%.(3) Valdecoxib increased the apoptosis rate from(14.15?0.48)% in control group to(29.80?6.35)% in treated group.(4) The expression of COX-2 mRNA and protein decreased in treated group compared with that in control group.FCM and immunohistochemical staining showed that the expressions of c-jun and c-fos were increased in valdecoxib treated group.There was statistical significance compared with control group.(5) There was significantly negative correlation between the ratio of apoptosis and the expression of COX-2(r=-0.726,P=0.008);there was significantly positive correlation between the ratio of apoptosis and the expressions of c-jun and c-fos protein respectively(r=0.603,0.813;P=0.038,0.001);(6) Valdecoxib did not affect cell structure of stomach and colon.Conclusions valdecoxib inhibits the growth of the xenograft tumor in nude mice and induces the apoptosis.Decreasing expression of COX-2 and up-regulating the expressions of c-jun and c-fos may be one of the mechanisms for the apoptosis.

Objective:To investigate the effects of TLR/STAT pathway in the proliferation of mesangial cell induced by HMGB1.Methods:Human mesangial cells were inoculated in the dose of 1?104 ml-1.After 24 h,cells were cultured with standard medium as control group or with medium supplement with 10 ?g/L human recombinant protein HMGB1 as trial group in vitro.Then the cells were collected in 6,12 and 24 h respectively,as well as control group cells.Immunocytochemical staining was adopted to examine the expressions of PCNA proteins on mesangial cells in different groups.Immunocytochemical staining and FCM were performed to detect the changes of TLR2 protein expression.STAT1 and STAT3 mRNA were examined by RT-PCR technique.Results:Immunocytochemical staining indicated that the mesangial cells could multiply after they were induced by human recombinant protein HMGB1.Immunocytochemical staining showed that the level of TLR2 protein in trial groups were higher than those in control groups.FCM indicated that HMGB1 could significantly up-regulate the expression of TLR2 protein time-dependently.The STAT1 and STAT3 mRNA in HMGB1 groups were higher than those in control groups.The expression of TLR2 protein was positively correlated with those of STAT1 and STAT mRNA respectively.The positive rate of PCNA was remarkably correlated with the expression of STAT1 and STAT3 mRNA.Conclusion:HMGB1 could activate STAT1/STAT3 through combining with its cell-surface receptor TLR2,which may play an important role in promoting the proliferation of mesangial cells and then damaging the renal of lupus nephritis.