This study is to investigate the protein and mRNA expressions of pro-inflammatory and anti-inflammatory cytokines in U937 foam cells and effects of Ginkgo biloba extract (GbE) on the cytokines.U937 cells were cultured with different concentrations of GbE (0.1,1,and 10 μg·L-1),and stimulated by 100 mg·L-1 oxidized low density lipoprotein (ox-LDL) for 24 h.The expressions of interleukin-1β (IL-1β),tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in culture solution were detected by enzyme-linked immunosorbant assay (ELISA) and reverse transcriptase polymerase chain reaction (RT-PCR).The results showed that incubated with 100 mg·L-1 ox-LDL for 24 h,the U937 cells became foam cells,the protein or mRNA expressions of IL-1β,TNF-α,IL-10,and its receptor IL-10R in U937 foam cells were higher markedly than those in normal U937 cells.When the cells were pretreated with GbE (0.1,1,and 10 μg·L-1),the increases of IL-1β and TNF-α in U937 foam cells were remarkably inhibited,but IL-10 expression increased greatly.Especially when cells were pretreated with 10 μg·L-1 GbE,the protein and mRNA expressions of IL-1β and TNF-α were markedly lower than those in U937 foam cells.The protein expression of IL-10 and mRNA expressions of IL-10 and its receptor IL-10R were markedly higher than those in U937 foam cells.GbE inhibited production of pro-inflammatory cytokines IL-1β and TNF-α,but up-regulated the production of anti-inflammatory cytokine IL-10 and its receptor IL-10R in U937 foam cells,which might be related with its anti-atherosclerotic actions.

Objective:To explore the protective effect of curcumin on type 2 diabetic nephropathy rats and the possible mechanism.Methods:30 Wistar rats were randomly divided into control group,the DN group and curcumin group,10 cases in each group,rats in DN and curcumin group were fed with high fat,after that they were used the streptozotocin injection to set up DN model.In addition,rats in curcumin group were given 200 mg/kg curcumin once a day,other two group were given sodium carboxymethylcellulose half-and-half.After 12 weeks,the 24 h urine were collected at the last delivery,the blood glucose(BG),total cholesterol(TC),triglyceride(TG),blood urea nitrogen(BUN),serum creatinine(Scr),microalbu minuria(mAlb) were tested,the urinary albumin excretion rate(UAER) was calculated.Furthermore,rats were sacrificed,kidney mass weighed,and the kidney index(KI) was calculated.Renal cortical was fixed with polymers cresol for hematoxylin-eosin(HE) staining,renal cortical was also made renal cortex homogenate and the SOD activity,MDA were detected,the expression of nuclear factor related factor 2(Nrf2) and heme oxygenase 1(HO-1) protein in the kidney tissues was detected with Western blot detection.Results:BG,TC,TG,KI,BUN,Scr,UAER,MDA of DN group and curcumin group were significantly higher than control group,and BM,KM,SOD was significantly lower than the control group,the amplitude raising or reducing in curcumin group were less than DN group,the difference had statistical significance(P<0.05);HE staining results showed that,compared with DN group,renal tubule degeneration in curcumin group was obviously reduced,inflammatory cells infiltration was decreased significantly;Western blot results showed that expression of Nrf2 and HO-1 protein in control group were significantly lower than DN group and curcumin group,and curcumin group was significantly higher than the DN group,the differences were statistically significant(P<0.05).Conclusion:Curcumin may play a role of kidney protection through the activation of Nrf2/ARE signaling pathway to reduce oxidative stress in diabetic nephropathy rats.

Objective To detect the expression and function of ZNRF3 in different kinds of thyroid cancer tissues and cells.Methods Immunohistochemistry was used to detect the expressions of ZNRF3 protein in 35 cases of papillary thyroid carcinoma and 10 cases of poorly differentiated thyroid carcinoma.The expressions of ZNRF3 gene in TPC-1 and 8505C were detected by RT-PCR,and the cell lines were derived from papillary thyroid carcinoma and poorly differentiated thyroid carcinoma respectively.After silenced ZNRF3 gene expression with lentivirus,the proliferation ability of TPC-1 cells were detected with CCK-8,the invasion and metastasis ability of TPC-1 cells were detected with Transwell.Results According to results of immunohistochemistry and RT-PCR,the expressions of ZNRF3 in papillary thyroid carcinoma cells and tissues were higher than those in poorly differentiated thyroid carcinoma cells and tissues,the differences were statistically significant (4.83±0.44 vs.3.13 ±0.59,t =2.20,P ＜0.05;1.01±0.06 vs.0.21±0.04,t =11.80,P＜0.01).After ZNRF3 geng silencing,according to the results of CCK8,the proliferation ability of TPC-1 cells was significantly enhanced in 72 h,the difference was statistically significant (0.96 ± 0.10 vs.0.64 ± 0.05,t =3.19,P ＜ 0.05);and according to the results of Transwell,the TPC-1 cell's invasion (0.12 ± 0.01 vs.0.09 ±0.00,t =5.48,P＜0.01) and migration (0.22 ±-0.01 vs.0.17 ±0.01,t =4.58,P ＜0.05) also increased,the differences were statistically significant.Conclusion The expression of ZNRF3 in papillary thyroid carcinoma is higher than that in poorly differentiated thyroid cancer.ZNRF3 is tumor suppressor gene in the thyroid tumors.

Electrocardiography ; Humans ; Long QT Syndrome

Objective: To investigate the possible mechanism of neuroprotection produced by taurine supplement on brain in young rats. Methods: In vitro, taurine treatment or co-treatment with sodium selenite that produced significant neuronal apoptosis was used in cultured cortical neurons to examine the neuroprotection effect using MTT assay and DNA fragmentation electrophoresis. In vivo, female weanling Sprague Dawley rats were divided into four groups, eight rats per group. The treated groups were fed on diets with different contents of taurine respectively, and the control group was fed on taurine unsupplemented diets. The experiment lasted five weeks. Results: Taurine significantly increased neuronal survival in dose-dependent manner. The typical DNA ladder pattern could be prevented by taurine. Taurine could elevate brain wet weight, and significantly increased the level of taurine, protein and AChE in brain. Conclusion: It is proposed that the neuroprotection effect of taurine could be achieved by modulating expression of related genes and blocking neuronal apoptosis.

T cell immunoglobulin and mucin domain 3 (Tim-3) is well known to negatively regulate T cells responses, but its role in burn-induced T cells immune suppression remains unclear. In the present study, in order to identify the relationship between Tim-3 expression and post-burn T cells immune suppression, C57BL/6 mice were subjected to burn injury or sham injury, and the liver and spleen were harvested at the day 1 after operation. The expression level of Tim-3 on hepatic or splenic T cells and the functional properties of Tim-3(+) T cells were evaluated. It was found burn injury induced dramatically elevated Tim-3 expression on both hepatic and splenic CD4(+) and CD8(+) T cells in contrast with the post-burn depletion of T cells. Furthermore, Tim-3 expression was correlated with the suppressive phenotype of T cells following burn injury, including increased expression of anti-inflammatory cytokine IL-10, decreased expression of pro-inflammatory cytokines IFN-γ and TNF-α, reduced T cell proliferation and elevated co-expression of Tim-3 and PD-1. Moreover, Tim-3(+) T cells subsets were more prone to spontaneous apoptosis than Tim-3(-) T cells subsets. Our findings reinforce the idea that the up-regulated expression of Tim-3 on T cells after burn injury plays an important role in the development and maintenance of burn-induced T cell immune suppression.

Objective To study the influence of high-fluoride on thyroid function and brain damage. Methods Thirty-six Wistar rats were randondy divided, according to weight and gender into 3 groups(12 rats each), i.e. control group, high fluoride group, and high fluoride plus thyroid tablet treatment group. The rats were fed with normal tap water containing no more than 5 mg/L NaF and the tap water added 100,100 mg/L NaF, respectively. After 7 months of experiment, the rats in high fluoride plus thyroid tablet treatment group were given with 0.04% thyroid tablet( 1.8 ml·kg~(-1)·d~(-1)) by gastric perfusion for three weeks. The contents of TT_3 and TT_4 in serum were detected by radio-immunological assay; the histomorphology in thyroids and brains were observed under microscopy; and the protein level of NMDAR2B subunit of glutamate receptor in the hippocampal CA1 and CA3 was measured by immunohistochemistry. Results As compared to the values of TT_3 and TT_4 in serum of rats in control group[ (0.97 ± 0.15), (84.03 ± 12.45)nmol/L], TT_3 and TT_4 in high fluoride group were obviously lower [(0.24 ± 0.07), (15.16 ± 2.08)nmol/L, all P < 0.01]; while no changes in TT_3 and TT_4 were detected in high fluoride plus thyroid tablet treatment group[ (1.02 ± 0.19), (85.63 ± 9.55)nmol/L, all P < 0.05] as compared to controls, but higher than those in high fluoride group(all P < 0.01 ). The pathological changes including partial hyperplasy, arrangement disorder, atrophy, and decreased colloid of the thyroid follicular epithelial cells in high fluoride group were observed under microscopy. In high fluoride plus thyroid tablet treatment group, the degree of the thyroid cellular hyperplasy was relatively slight as compared to high fluoride group. The swelling and disarrangement of neurons in the hippocampus were observed in high fluoride group, whereas the changes of the neurons were not so obvious in high fluoride plus thyroid tablet treatment group. The grey values of NMDAR2B positive cells in the hippocampal CA1 and CA3 in high fluoride group(167.05 ± 7.31 ) were significantly increased as compared to controls (92.53 ± 9.67 ) or high fluoride plus thyroid tablet treatment group( 101.66 ± 12.21, all P < 0.01 ). Conclusions High fluoride can induce the decreased function and changed histomorphology in thyroid and result in pathological damages in the brains of rats. However, treated with thyroid tablet to those having damages induced by high fluoride, the thyroid function and morphology can be normal, and the brain damages can be alleviated. The results indicate that hypothyroidism caused by high fluoride might be an important participating factor in brain damages caused by fluorosis.

Aim To investigate the effects of panax nonstaining saponins ( PNS ) on the apoptosis of renal cells induced by cisplatin through the path of mitochon-drion . Methods Male Sprague-Dawley( SD) rats were randomized divided into normal control group, cisplatin model group and the cisplatin+PNS group,with 12 rats of each group. Animals were sacrificed to determine the N-acetyl-β-D-Glucosaminidase ( NAG ) in urine, blood urea nitrogen ( BUN) and serum creatinine ( Cr) concentrations after 8d of intraperitoneal injection. HE-staining was employed to observe renal pathologies. Transmission electron microscopy ( TEM ) was em-ployed to observe the mitochondria of the rats′ injured kidney region. TUNEL staining was employed to detect the distribution of apoptotic cells. Immunnohistochem-istry was used to detect Bax and caspase-9 expression, and expression of Bcl-2 protein was detected by West-ern blot. Results Compared with the normal control group, contents of BUN, serum Cr and urinary NAG levels of rat in the cisplatin model group were increased ( P <0. 01 ) , and some mitochondria of the epithelial cells of renal tubules got injured seriously. The apopto-sis rate of kidney cell was increased ( P<0. 01 ) . The expression of Bax,caspase-9 and Bcl-2 proteins was in-creased ( P < 0. 01 ) . Compared with the cisplatin model group, contents of BUN, serum Cr and urinary NAG levels of rats in the cisplatin model group were decreased ( P <0. 01 ) , and some mitochondria of the epithelial cells of renal tubules were significantly im-proved. The apoptosis rate of kidney cell was decreased ( P<0. 01 ) . The expression of Bax and caspase-9 pro-tein was decreased (P<0. 01),but Bcl-2 protein was increased ( P < 0. 01 ) . Conclusion PNS may in-crease the expression of Bcl-2 protein and decrease the expression of Bax and caspase-9 proteins, which may play a protective role in cisplatin nephritic damage.

As an important part of traditional Chinese medicine (TCM), mineral medicine plays an irreplaceable role. However, little has been reported on its species and valence state of heavy metals and deleterious elements, and also the relevance to pharmacological effect and toxicology. The present paper, in a new perspective, summarized the determination of the species and valence state of heavy metals and deleterious elements in recent years, discussed the progress of the pharmacological effect and toxicology, and prospected for future study which might provide reference for mineral medicine.
Animals ; Drug Contamination ; statistics & numerical data ; Drug Therapy ; Humans ; Medicine, Chinese Traditional ; Metals, Heavy ; analysis ; toxicity ; Minerals ; analysis ; pharmacology

Objective To investigate the potential clinical factors associated with the prognosis and relapse of adult onset Still's disease(AOSD).Methods The factors possibly influencing the prognosis and relapse of AOSD were analyzed by logistic regression and COX regression in the cohort study.Ninety-six con- secutive inpatients of AOSD diagnosed based on Yamaguchi criteria in the hospital from March 1996 to September 2004 were included in the study.Results Nine cases(9.4%)were lost during the follow-up. Eleven patients(12.6%)were diagnosed as other diseases(5 with other rheumatic diseases,4 with tumor and 2 with infections)in the 87 follow-up cases.In 76 cases,3 patients(3.9%)died and 33 patients(43.4%) got remission over one year after treatment.Splenomegaly(OR=3.14,95%CI=1.01～9.74)and treated with methotrexate(OR=0.22,95%CI=0.07～0.67)were associated with the prognosis from the logistic regression analysis of the 76 cases.The serum ferritin(RR=I.05,95%CI=1.01～1.08)and treated with methotrexate (RR=0.13,95%CI=0.02～0.76)were associated with relapse from the COX regression analysis of the 61 remis- sion cases.Conclusion We need to be very cautious in the follow-up of AOSD patients because some of them may change to other diseases.Methotrexate may be an importent therapy of AOSD not only in improve- ment the prognosis but also in reduction of relapse.