Objective To investigate the effect of Saussurea involucrata Injection(SII)on counteracting adjuvant-induced arthritis and its immunoregulation function,thus to supply the pharmacological evidences for the clinical treatment of arthritis.Methods Adjuvant arthritis was induced by plantar injection of Freundi' s complete adjuvant.MTT method was used to detect T and B lymphocytes proliferation,and sheep red blood cell immunization was used for hemolysin determination.Results(1)Rats right posterior metatarsus which was injected adjuvant was swollen from the second day to the 22nd day(the primary injury),and left posterior metatarsus not receiving adjuvant injection was swollen from the sixth day to the 20 th day(the secondary lesion).The differences of swelling degree were significant between SII group and NS group.(2)Consecutive intramuscular injection of SII 0.2,0.4,0.8 mL? kg-1? d-1 for 22 days suppressed the primary injury and the secondary lesion of adjuvant arthritis in rats,relieved swelling significantly from the sixth day(P

Objective To investigate the expression of CK19mRNA and CD44mRNA in peripheral blood of patients with breast cancer for forecasting micrometastasis. Methods Expression of CK19 and CD44 were detected in 107 patients by RT-PCR method. Results CK19 and CD44 were positive in 31.8%(34/107) and 32.7%(35/107) of patients with breast cancer 24 hours before surgery respectively,which were statistically different from that of 12 days postoperatively and that of normal controls (all P

Aim To investigate the protective effects of chrysophanol( Chry) on immune function of lead poi-soning mice. Methods The lead poisoning model was established by peritoneally injecting mice with 7 mg · kg-1 lead acetate every day for 8 days. After Chry was ip injected for 14 days,spleen and thymus index, the white blood cell count, T, B lymphocyte proliferation, phagocytic function of macrophages, natural killer cell ( NK cell) activity were detected. The concentrations of IFN-γ,IL-2,IL-4,IL-10 in the lead poisoning mice ser-um were determined by enzyme-linked immunosorbent assay ( ELISA) . Results Intraperitoneal injection of 7 mg · kg-1 lead acetate for 8 consecutive days could cause an immunity decline in lead poisoning mice, Chry could significantly improve the immunity of lead poisoning mice. Compared with model group, Chry sig-nificantly improved growth rate, viscera index and white blood cell count of lead poisoning mice at differ-ent extent ( P<0 . 05 or P<0. 01 ) . Chry ( 1 . 0 ,10 . 0 mg·kg-1 ) significantly increased the B,T lymphocyte proliferation ( P<0 . 01 ) and the phagocytosis of macro-phage and NK cell activity ( P <0 . 01 ) . Compared with the control group, the concentrations of IFN-γ, IL-2 , IL-4 , IL-10 of lead poisoning mice serum were significantly reduced ( P <0 . 01 ) . Compared with the model group, Chry (1. 0、10. 0 mg·kg-1 ) significant-ly increased the concentrations of IFN-γ, IL-2 , IL-4 , IL-10 ( P <0. 01 ) , while there were no significant changes in (0. 1 mg·kg-1 ) concentrations of IFN-γ, IL-2 , IL-4 in Chry ( 0 . 1 mg · kg-1 ) treatment group ( P>0. 05 ) , only IL-10 was significantly increased in Chry ( 0 . 1 mg · kg-1 ) treatment group ( P<0 . 05 ) . Conclusion Chry can significantly improve the im-mune function of lead poisoning mice.

Insulin resistance in insulin sensitive organ results in metabolic disorder such as hyperglycemia, hyperinsulinemia and hyper triglyceridemia which are common features of type 2 diabetes.Insulin resistance in liver cells mainly causes impaired glycogen synthesis, failed to suppress glucose production which is the major contribution to hyperglycemia.FGF-21 as a new metabolic regulator can control fasting blood glucose.The mechanism of FGF-21 effects on regulating plasma glucose has little to known.In order to establish an in vitro insulin resistant model of liver cells and evaluate the effects and mechanism of FGF-21 on glucose metabolism in the cell model, HepG2 cells were incubated with 10-7 mol/L insulin for 24 h to build insulin-resistant cell model.To evaluate the cells for insulin resistance, the cells were stimulated with fresh insulin for 24 h and the glucose uptake by these cells was carried out.The insulin-resistant cells were treated with different concentrations of FGF-21 for 24 h and insulin-treated cells were used as a control.The glucose uptake by the cells was detected by the method of glucose oxidizes/peroxides(GOD-POD);the synergy between insulin and FGF-21 was evaluated.The mRNA expression of GLUT1 in the insulin-resistant cells was detected by the real-time PCR.Glycogen synthesis of the cells was examined by the anthrone method.The results showed that HepG2 cells treated with 10-7 mol/L insulin for 24 h became resistant to insulin and the insulin resistance status was maintained for 48 h without change of cell morphology.FGF-21 could stimulate glucose consumption of the insulin-resistant model in a dose-dependent manner.The glucose consumption and glycogen synthesis of the insulin-resistant model were significantly improved by FGF-21 treatment.FGF-21 showed strong synergy with insulin in glucose uptake and glycogen synthesis of the model cells.While the cells became resistant to insulin, FGF-21 could increase the mRNA expression of GLUT1.Thus, It is concluded that FGF-21 stimulates glucose uptake in insulin resistant HepG2 cells through GLUT1 expression, stimulates glycogen synthesis and improves the glucose metabolism in the insulin resistant liver cell model.

Aim Carvacrol ( CAR ) , possesses a wide variety of pharmacological properties including antioxi-dant and anti-inflammatory potential. The present stud-y is designed to investigate the effect of CAR on glu-cose and lipid metabolism in type 1 diabetic mice. Methods Diabetes was induced by intraperitoneal( i. p) injection of streptozotocin into male mice at the dose of 45 mg·kg-1 body weight( BW) . Mice were divided into three different groups containing eight to twelve in each. Age matched male C57 mice were used as nor-mal controls. Group I diabetes, Group Ⅱ and Ⅱ in-jected with CAR at 10 and 20 mg · kg-1 BW respec-tively once daily. After CAR injection 2, 4 or 6 weeks, the rats were weighted and the plasma concen-trations of glucose, total cholesterol( TC) , triglycerides (TG), Glutamic oxalacetic transaminase(AST), Ala-nine transaminase( ALT) levels were enzymatically de-termined using commercial kits. Results STZ-induced C57 BL/6 J diabetic mice showed an elevation in serum glucose, TG, ALT, AST and LDH levels. Compared to diabetic mice, administration of CAR resulted in sig-nificant decreases(P <0. 05) in plasma glucose, TG and LDH levels in a dose dependent manner, but no effect on elevated TC, ALT and AST levels. Conclu-sion These major findings provide evidence that CAR has anti diabetic property and it has the potential for development into a drug to prevent hyperglycemia, re-duce blood lipids and protect the dammaged organs.

Objective To investigate the effects of dexmedetomidine on the proliferation and auto-phagy of human colon cancer cells.Methods In experiment 1,human colon cancer cells LoVo and HCT116 were selected and divided into eight groups:LoVo-1 group(group L0-1),LoVo+dexmedetomi-dine 1 nmol/L-1 group(group L1-1),LoVo+dexmedetomidine 10 nmol/L-1 group(group L10-1),LoVo+dexmedetomidine 100 nmol/L-1 group(group L100-1),HCT116-1 group(group H0-1),HCT116+dexmedetomidine 1 nmol/L-1 group(group H1-1),HCT116+dexmedetomidine 10 nmol/L-1 group(group H10-1)and HCT116+dexmedetomidine 100 nmol/L-1 group(group H100-1).The cell proliferation rate was detected by CCK-8 method 24 and 48 hours after drug treatment.The cells were collected 24 hours after drug treatment,and the contents of microtubule-associated protein 1 light chain 3(LC3)-Ⅱ and autophagy associated protein Beclin-1 were detected by Western blot method.In experiment 2,LoVo and HCT116 were selected and divided into four groups:LoVo-2 group(group L0-2),LoVo+dexmedetomidine 10 nmol/L-2 group(group L10-2),HCT116-2 group(group H0-2)and HCT116+dexmedetomidine 10 nmol/L-2 group(group H10-2).Cells were collected 24 hours after drug treatment,LC3 protein expression was observed by immunofluorescence method,and the positive rate of LC3 site was calculated.The autophagosomes were col-lected and observed by transmission electron microscopy 24 hours after drug treatment.Results In experi-ment 1,the cell proliferation rate in groups L10-1 and L100-1 was significantly lower than that in groups L0-1 and L1-1 24 and 48 hours after drug treatment,the protein content of LC3-Ⅱ and Beclin-1 was signifi-cantly higher than that in groups L0-1 and L1-1 24 hours after drug treatment(P＜0.05).The cell prolifer-ation rate in groups H10-1 and H100-1 was significantly lower than that in groups H0-1 and H1-1 24 and 48 hours after drug treatment,and the protein content of LC3-Ⅱ and Beclin-1 was significantly higher than that in groups H0-1 and H1-1 24 hours after drug treatment(P＜0.05).In experiment 2,compared with group L0-2,the positive rate of LC3 site in group L10-2 was significantly increased 24 hours after drug treatment(P＜0.05).Compared with group H0-2,the positive rate of LC3 site in group H10-2 was significantly in-creased 24 hours after drug treatment(P＜0.05).Groups L0-2 and H0-2 have intact cell membranes and clear nuclei.The cell membrane in groups L10-2 and H10-2 was damaged,the arrangement of organelles was disordered,and a large number of autophagosomes and autophagosomes were visible.Conclusion Dexmedetomidine may inhibit the proliferation of colon cancer cells by inducing autophagy.

[Objective]To explore how hyperthyroidism induces ventricular remodeling via activating β-catenin/FoxO1 in rat cardiomyocytes.[Methods]Hyperthyroidism-induced ventricular remodeling rat models were established by intraperitoneal injection of levothyroxine(T4)at 0.1 mg/kg for 30 days.β-catenin inhibitor MSAB(14 mg/kg)was admin-istrated for 30 days.We used western blot to detect the expression of myocardial hypertrophy marker ANP,β-catenin and FoxO1;immunofluorescence to examine the expression and intracellular distribution of β-catenin and FoxO1.Hyperthy-roidism-induced cardiomyocyte hypertrophy rat models were established by treatment of triiodothyronine(T3)into cul-tured primary neonatal rat cardiomyocytes for 24 hours.β-catenin siRNA(30 nmol/L)was used to down-regulate β-catenin expression in cardiomyocytes.Western blot and immunofluorescence were used to analyze the effects of β-catenin inhibition on the hyperthyroidism-induced cardiomyocyte hypertrophy.[Results]Following Wnt/β-catenin activation,β-catenin was found increased nuclear expression,to bind to the nuclear transcriptional factors and regulate the gene ex-pression.β-catenin nuclear expression was significantly increased in the hyperthyroidism-induced ventricular remodeling rats,but no change was found in the expression of typical transcriptional factor TCF7l2.Our results revealed that inhibiting β-catenin by MSAB attenuated the hyperthyroidism-induced rat ventricular remodeling.Further analysis indicated that β-catenin/FoxO1 expression was significantly increased in hyperthyroidism-induced myocardial hypertrophy which could be attenuated by suppressing β-catenin/FoxO1 in cardiomyocytes.[Conclusions]β-catenin/FoxO1 is activated in hyperthy-roidism-induced myocardial hypertrophy and β-catenin/FoxO1 inhibition attenuates hyperthyroidism-induced cardiomyo-cyte hypertrophy.