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.

Cell Line, Tumor ; Humans ; Leukemia-Lymphoma, Adult T-Cell ; metabolism ; NF-kappa B ; metabolism ; Proto-Oncogene Proteins ; metabolism ; Transcription Factors ; metabolism

Objective To study the clinical and electrophysiological characteristics of peripheral neuropathy in patients with multiple sclerosis(MS).Methods As a total of 84 MS patients,the clinical and electrophysiological data were analyzed in 16 MS patients with the symptoms of peripheral neuropathy(PNMS group)and in 68 MS patients without peripheral neuropathy(NPNMS group).Results The incidence of peripheral neuropathy was 19.0%(16/84)in this group.The clinical symptoms included extremity numbness in 14 cases(87.5%),limb inertia in 12 cases(75.0%),and radicular pain in 4 cases(25.0%).Signs included decrease of tendon reflex in 15 cases(93.7%),periphery sensory disability in 13 cases(81.2%),and myatrophy in 5 cases(31.2%).The mean age in the PNMS group was(44.6?12.5)years vs.(32.2?11.5)years in the NPNMS group.The course of disease was(39.3?18.3)months vs.(31.6?17.2)months in the NPNMS group,there were significant differences in two groups(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.

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 relation-ship 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.