Aim To investigate the effects of curcumin on expression of HIF-1? in human hepatocellular carcinoma BEL-7402 cells.Methods Different concentrations of 0,2.5,5,10,15 and 20 ?mol?L~(-1) curcumin-treated human hepatocellular carcinoma BEL-7402 cells were cultured under hypoxia for 6 hours.The cell proliferation and cell viability were assayed by WST-8 and the trypan blue dye exclusion method.The expression level of HIF-1? in human hepatocellular carcinoma BEL-7402 cells was checked by RT-PCR and Western Blot;0,10 ?mol?L~(-1) curcumin,10 ?mol?L~(-1) MG-132,and 10 ?mol?L~(-1) curcumin +10 ?mol? L~(-1) MG-132-treated human hepatocellular carcinoma BEL-7402 cells were cultured under hypoxia for 6 hours.The protein expression level of HIF-1? protein in human hepatocellular carcinoma BEL-7402 cells was checked by Western Blot.Results ① No significant difference was found in the cell proliferation rate and cell viability between control and different concentrations of curcumin.② Curcumin can down-regulate the expression of HIF-1? protein with the increasing concentrations.③ the effect of curcumin on expression of HIF-1?mRNA had no significant difference between control and different concentrations.④ MG-132 can reverse the curcumin-mediated decrease of HIF-1? protein.Conclusion Inhibitory effect of curcumin on expression of HIF-1? in human hepatocellular carcinoma BEL-7402 cells was acted through posttranscriptional mechanisms and the proteasome pathway.

Hemoperfusion ; Humans ; Metabolic Clearance Rate ; Paraquat ; blood ; pharmacokinetics

Adult ; Case-Control Studies ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; blood ; immunology ; T-Lymphocyte Subsets

The paper aims to study the pharmacokinetic parameters of gastrodin in rats effected by compound compatibilitiy and different doses of Tiangou Jiangya capsule. The extracts from Gastrodiae Rhizoma( equivalent to gastrodin 16.82 mg x kg(-1) and Tiangou jiangya capsule (equivalent to gastrodin 8.410, 16.82, 33.64 mg x kg(-1)) were oral administrated to rats respectively. The plasma were taken at various time points and treated with acetonitrile to measure the contents of gastrodin by HPLC method. The mean plasma concentration-time data were analyzed by 3P97 pharmacokinetic software and the pharmacokinetic parameters between groups were treated by SPSS 16.0. The results showed that gastrodin in rat was fitted to one-compartment model, Cmax and AUC of Tiangou Jiangya capsule were in direct proportion to oral administration, and t1/2Ka had nothing to do with doses, which indicated that gastrodin was fitted first-order rate transfter process in vivo. Morever, comparison with the Gastrodiae Rhizoma extract, isodose gastrodin in Tiangou Jiangya capsule showed a significant decrease for Cmax, Ke and increase for t1/2Ke, V/Fc, this indicated that compound compatibility can delay the absorbtion of gastrodin, prolong the resident time and promote the distribution in vivo, but its bioavailability is not significantly effected.
Administration, Oral ; Animals ; Benzyl Alcohols ; administration & dosage ; chemistry ; pharmacokinetics ; pharmacology ; Blood Pressure ; drug effects ; Female ; Flavonoids ; chemistry ; pharmacology ; Furans ; chemistry ; pharmacology ; Gastrodia ; chemistry ; Glucosides ; administration & dosage ; chemistry ; pharmacokinetics ; pharmacology ; Lignans ; chemistry ; pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Software

Blood Cells ; immunology ; pathology ; Bone Marrow Cells ; immunology ; pathology ; Child, Preschool ; Diagnosis, Differential ; Female ; Humans ; Immunophenotyping ; Leukemoid Reaction ; diagnosis

Objective To study the effect of calcium on human peritoneal mesothelial cells (HPMCs). Methods Proliferation abilities of HPMCs were assessed by tetrazolium salt colorimetry assay (MTT assay) and the levels of LDH in the supernatant were detected in all groups to evaluate the damage of HPMCs. The expression of TNF-α in cytoplasm was detected by immunohistochemistry. Results Calcium enhanced proliferation of HPMCs in a time-dependent manor(P＜0.01), especially calcium with 1.25 mmol/L(0.5098±0.016,0.6763±0.048) and 1.0 mmol/L(0.4853±0.016,0.6678±0.076). Calcium with different concentrations significantly increased the levels of LDH in HPMCs in a time-dependent manor, while the effect of calcium with 1.25 mmol/L was lowest(17.78±1.18,23.60±1.39,P＜0.01). Calcium with 2.0 mmol/L[(42.61±3.29)%] and 1.75 mmol/L[(33.32±1.88)%] significantly up-regulated the expression of TNF-α(P＜0.01) . Conclusions High calcium damaged HPMCs and up-regulated the expression of TNF-αby HPMCs, while physical calcium (1.25 mmol/L)can protect peritoneum and prevent peritoneal fibrosis.

Mitogen activated protein kinase(MAPK)is one of the four biggest signal transduction systems which contain four subtribes named p38,ERK5/BMK1,ERK and JNK/SAPK respectively.Previous studies have shown that MAPK pathway is involved in growth,cell differentiation,perishing,the synchronization of cell function and so on.ERK/MAPK,one of the members of MAPK family,and Sma-and MAD-related(Smad)play important roles in the proliferation of fibroblast,modulating inflammation mediator production as well as transferring factors activity in the process of pulmonary fibrosis(PF).This review focuses on relationship between Smads and ERK in the pathogenesis and progression of PF.

Objective To explore the change of serum level of neuron specific enolase (NSE) in neonates with asphyxia before and after head mild hypothermia.Methods Eighty-two asphyxial neonates were selected,including 39 mild asphyxial neonates and 43 severe asphy-xial neonates,and 29 healthy neonates were selected as control group.Forty-three severe asphyxial neonates were randomly assigned into mild hypothermia treatment group and traditional treatment group.Neonates in traditional treatment group were just given traditional treatment.While neonates in mild hypothermia treatment group received head mild hypothermia therapy and their nasopharyngeal temperature were maintained at(34.0 ? 0.5) ℃ for 72 h.Before treatment and 72 h after treatment,2 mL blood was collected,and the serum NSE was determined by radio immunoassay.Results NSE levels in mild asphyxial neonates group[(34.83?6.17) ?g/L] and severe asphyxial group[(59.58?8.87) ?g/L] were significantly higher than that of control group[(30.57?4.88) ?g/L](t=3.07 P0.05).The level of NSE at 72 h in severe asphyxial neonates with head mild hypothermia therapy[(40.97?6.55) ?g/L] was significantly lower than that of traditional treatment group [(48.15?5.57) ?g/L](t=3.86 P

Objective To investigate the related risk factors and neonatal outcomes in early preterm birth by analysis of 198 cases of early-to-moderate preterm birth. Methods Retrospective analysis was conducted on 198 pregnant women hospitalized during January 2004 to September 2006 with early-to-moderate preterm birth who delivered at 28 to 33+6 weeks of gestational age and their preterm infants.All of them were divided into two groups: early preterm birth group,28 to 3l+6 weeks of gestational age,n=90 for the pregnant women and n= 99 for the preterm infants;moderate preterm birth group,32 to 33+6 weeks of gestational age,n=108 for the pregnant women and n=122 for the preterm infants(fatal birth defects were excepted).The risk factors for preterm birth and neonatal outcomes were compared between the two groups. Results Various factors contributed to the occurrence of preterm birth.Systemic antenatal care and weight gain during pregnancy were significantly less found in the early preterm birth group than the moderate preterm birth group(P

Liver fibrosis can be caused by chronic liver injury arising from various etiological factors and it is a reversible process.The activation of the hepatic stellate cell(HSC)is the central event in liver fibrosis,since we know that cytokines secreted from Kupffer cell participate in HSC proliferation,apoptosis and ECM metabolism.In this paper we focus on the relationship between HSCs,Kupffer cell,cytokines and the course of hepatic fibrosis.Elucidating this relationship will benefit research on the role of Kupffer and HSCs in hepatic fibrosis.