Objective To explain the effects of C-reactive protein(CRP) on lectin-like oxidized low density lipoprotein receptor-1 expression on THP-1 derived macrophages and the related signal transduction pathways.MethodsTHP-1 cells were differentiated into macrophages with the stimulation of PMA.THP-1 derived macrophages were incubated with CRP and co-incubated with inhibitors of NF-?B、AP-1 and MARK signal transduction pathways.The expression of LOX-1 antigen and mRNA was analyzed by ELISA and RT-PCR.Results CRP stimulated the expression of LOX-1 antigen and mRNA on macrophages in a dose-dependent manner.NF-?B inhibitor BAY11-7085 suppressed the inducible effects of CRP on LOX-1 expression.Conclusion CRP increased LOX-1 expression on THP-1 derived macrophages at transcription and post-transcription levels.The NF-?B signal transduction pathway may be involved in such process.

Objective To observe the effects of mild hypothermia induced by pentobarbital sodium on hematology in male BALB/C mice.Method Healthy male BALB/C mice were divided randomly into two groups:control group ( C) and mild hypothermia group(M).The body temperature of the mild hypothermia group was maintained between 28℃ to 30℃( anal temperature ) for 4 hours induced by pentobarbital sodium injected intraperitoneally , then recover unaffected . Anal temperature, coagulation, electrolytes, and blood cell indexes were examined in 2, 24, 72 hours after treated by mild hypothermia;Control group was given equal volume of saline volume at constant temperature .Results The body temperature and coagulation in mild hypothermia group showed no significant difference compared with the control group ( P﹥0.05),but the concentration of K +and Na +in mild hypothermia group were higher than control group (P﹤0.01), the number of WBC in mild hypothermia group was lower than control group ( P﹤0.01或P﹤0.05 ) , and the RBC、HGB、MCH、MCHC in mild hypothermia group were lower than control group transiently (P﹤0.01或P﹤0.05).Conclusion Mild hypothermia induced by pentobarbital sodium affects some of hematological values in mice considerably .

Objective To explore the effects of microRNA(miR)-1283 on invasion,proliferation and apoptosis of HTR 8/SVneo cell line derived from human-trophoblast cells.Methods HTR-8/SVneo cells were divided into three groups,as-miR 1283 group was transfected with miR 1283 analogues,anti-miR-1283 group was transfected with miR-1283 inhibitors,and negative control group was transfected with non functional sequence.The levels of miR 1283 expression were detected by fluorescence quantitative polymerase chain reaction at 24 hours after transfection.The cell proliferation was measured by 3-(4,5)-dimethylthiazol-2-yl-(2,5)-diphenyl tetrazolium bromide assay at 24,48 and 72 hours after transfection.Apoptosis was evaluated by propidium iodide staining and flow cytometry at 48 hours after transfection.Transwell experiments were performed to evaluate cellular invasion abilities at 24 hours after transfection.Analysis of variance and Bonferroni method were applied as statistical methods.Results The level of miR 1283 in as miR 1283 group was higher than that in the negative control group with statistically significant difference (14.85±0.57 vs 7.08±0.20,P＜0.01).At 24,48 and 72 hours after transfection,the inhibitory rate of cell proliferation in as-miR-1283 group was (8.04 ± 0.27) ％,(32.47 ± 0.24) ％ and (9.23± 0.17) ％,higher than those in the negative control group [(0.72 ± 0.06) ％,(1.17 ± 0.04) ％ and (0.53 ± 0.05) ％] (P ＜ 0.01,respectively).Cell apoptosis rate was higher in as-miR 1283 group than in negative control group [(16.33 ± 0.40) ％ vs (9.39± 0.58) ％,P＜0.01].The transmembrane cell number was lower in as-miR-1283 group as comparing with the negative control group (7.25 ± 1.83 vs 16.33 ± 2.08,P＜0.01).miR-1283 expression,apoptosis and transmembrane cell number in anti-miR-1283 group had no statistical difference as compared to the negative control group (all P ＞ 0.05).Conclusions Up-regulated levels of miR-1283 could inhibit HTR-8/SVneo cell proliferation and invasion,but promote the cell apoptosis.

OBJECTIVETo observe the relation between Pi deficiency syndrome (PDS) and the configuration and functions of extensor digitorum longus (EDL)and soleus (SOL).

METHODSTotally 36 ICR mice were randomly divided into 3 groups according to weight matching principle, the control group, the exhausted group, and the rhubarb group, 12 in each group. Two PDS models were established by either purgation with rhubarb diarrhea (as Group A) or exhausted swimming plus sleep deprivation (as Group B).The cross sectional area (CSA) of type I and II fibers of extensor digitorum longus (EDL) and soleus (SOL), relative proportions of type I and II fibers were measured by m-ATPase histochemical method. The isotonic contraction and the maximum tetanus contraction of EDL and SOL were detected by PowerLab system.

RESULTSCompared with the control group, the body weight, body temperature, and the general health condition of PDS model rats obviously decreased; the spleen index and the thymus index were also lower; the maximal isotonic contraction and the maximum tetanus contraction obviously decreased; the cross section areas of EDL and SOL were reduced with loosely arranged cells. In EDL, the proportion of type I fibers was added and the proportion of type II fibers was lowered. In SOL, there was no change in the proportion of type I and type II fibers.

CONCLUSIONSEDL and SOL were obviously atrophied in the two PDS model mice. The type I fibers of SOL was more significantly atrophied in Group B.

This study is to evaluate the effects of the metformin (Met) on β cell function of diabetic KKAy mice. Female diabetic KKAy mice selected by insulin tolerance test (ITT) were divided randomly into two groups. Con group was orally administered by gavage with water, Met group with metformin hydrochloride at a dose of 0.2 g x kg(-1) for about 12 weeks. ITT and glucose tolerance tests (OGTT) were determined. Beta cell function was assessed by hyperglycemic clamp. Pancreatic biochemical indicators were tested. The changes of gene and protein expression in the pancreas and islets were also analyzed by Real-Time-PCR and immunostaining. Met significantly improved glucose intolerance and insulin resistance in KKAy mice. Fasting plasma glucose and insulin levels were also decreased. In addition, Met markedly increased glucose infusion rate (GIR) and elevated the Ist phase and maximum insulin secretion during clamp. It showed that Met decreased TG content and iNOS activities and increased Ca(2+) -Mg(2+)-ATPase activity in pancreas. Islets periphery was improved, and down-regulation of glucagon and up-regulated insulin protein expressions were found after Met treatment. Pancreatic mRNA expressions of inflammation factors including TLR4, NF-κB, JNK, IL-6 and TNF-α were down-regulated, p-NF-κB p65 protein levels also down-regulated by Met. And mRNA expressions of ion homeostasis involved in insulin secretion including SERCA2 and Kir6.2 were up-regulated by Met. Met increased SIRT5 expression level in pancreas of KKAy mice under the hyperglycemic clamp. These results indicated that chronic administration of Met regulated pancreatic inflammation generation, ion and hormone homeostasis and improved β cell function of diabetic KKAy mice.
Animals ; Blood Glucose ; Diabetes Mellitus, Experimental ; drug therapy ; Down-Regulation ; Female ; Glucose Tolerance Test ; Homeostasis ; Inflammation ; drug therapy ; Insulin ; secretion ; Insulin Resistance ; Insulin-Secreting Cells ; drug effects ; Interleukin-6 ; metabolism ; Metformin ; pharmacology ; Mice ; NF-kappa B ; metabolism ; Pancreas ; drug effects ; Tumor Necrosis Factor-alpha ; metabolism

AIM: To assess the relative agreement of GAT and NCT in IOP measurement by comparing the differences between Goldmann applanation tonometer (GAT) and non-contact tonometer (NCT) in intraocular pressure (IOP) detection.METHODS: IOP of 529 eyes of 265 volunteers were measured with both NCT and GAT, respectively.RESULTS: The measurement results of NCT were lower than that of GAT, there was significant difference between the IOP measured with NCT and GAT (19.13 vs23.43, t=22.644, P＜0.05). With the increasing of IOP values, the difference magnitude was greater, especially in IOP group that was more than 30mmHg, but the correlation coefficient became lower.CONCLUSION: The measurement results with NCT are lower than that of GAT. When the IOP with the NCT is in borderline value, it need be corrected with GAT, in order to discover the pathologically elevated IOP and avoid the misdiagnosis and mistreatment of glaucoma.

This study is to evaluate the effects of the metformin (Met) on β cell function of diabetic KKAy mice. Female diabetic KKAy mice selected by insulin tolerance test (ITT) were divided randomly into two groups. Con group was orally administered by gavage with water, Met group with metformin hydrochloride at a dose of 0.2 g x kg(-1) for about 12 weeks. ITT and glucose tolerance tests (OGTT) were determined. Beta cell function was assessed by hyperglycemic clamp. Pancreatic biochemical indicators were tested. The changes of gene and protein expression in the pancreas and islets were also analyzed by Real-Time-PCR and immunostaining. Met significantly improved glucose intolerance and insulin resistance in KKAy mice. Fasting plasma glucose and insulin levels were also decreased. In addition, Met markedly increased glucose infusion rate (GIR) and elevated the Ist phase and maximum insulin secretion during clamp. It showed that Met decreased TG content and iNOS activities and increased Ca(2+) -Mg(2+)-ATPase activity in pancreas. Islets periphery was improved, and down-regulation of glucagon and up-regulated insulin protein expressions were found after Met treatment. Pancreatic mRNA expressions of inflammation factors including TLR4, NF-κB, JNK, IL-6 and TNF-α were down-regulated, p-NF-κB p65 protein levels also down-regulated by Met. And mRNA expressions of ion homeostasis involved in insulin secretion including SERCA2 and Kir6.2 were up-regulated by Met. Met increased SIRT5 expression level in pancreas of KKAy mice under the hyperglycemic clamp. These results indicated that chronic administration of Met regulated pancreatic inflammation generation, ion and hormone homeostasis and improved β cell function of diabetic KKAy mice.

Objective To study the effect of different concentration of 1,25-dihydroxyvitamin D3[1,25(OH)2D3] on cell proliferation,differentiation and the expression of vitamin D receptor (VDR) in mouse MC3T3E1 osteoblast.Methods Osteoblast were cultured in medium with different concentrations of 1,25(OH)2D3.Incubated for 48 h,cell proliferation of osteoblast were examined by MTT reduction assay (mono-nuclear cell direc cytotoxicity assay),the osteocalcin (OC) levels in cell medium were detected by ELISA,and the expression of VDR mRNA and protein were examined by using SYBR Green real-time PCR and Western blot,respectively.Results 1.After incubation with 1,25(OH)2D3 for 48 h,the number of MC3T3E1 osteoblast was significantly less than that in control group(P0.05).3.SYBR Green real-time PCR and Western blot results showed that the expression of VDR mRNA as well as VDR protein of osteoblast in 10-8,10-9 mol/L experimental groups were significantly higher than those in control group (Pa0.05).Conclusions Cell proliferation of mouse osteoblast can be inhibited,while the cell differentiation was promoted by 1,25(OH)2D3.1,25(OH)2D3 up-regulated the expression of VDR in mouse osteoblast,which suggested that the VDR signal pathway may play some role in proliferation and differentiation of osteoblast.

Objective To explore the interaction characters of fluoride and aluminum by analyzing the changes of bone metabolism in mice. Methods Kunming mice were randomly divided into nine groups according to the factorial experiment, design of two factors and three levels. The animals in different groups were fed with various doses of fluoride(NaF, 0,50,150 mg/L) and/or aluminum(AlCl3, 0,200,600 mg/L) in drinking water for 24 weeks. Serum calcium, phosphor, magnesium, alkaline phosphatase, osteoealine, parathyroid, and urinary calcium and phosphor were tested. Results We found interaetians of fluoride and aluminum with serum calcium, osteoealine and urine calcium(F=17.370,4.399,9.448, P<0.01), but not with serum phosphor, magnesium, alkaline phosphatase, parathyroid or urinary phospbor(F=0.416,0.415,1.921,1.362, 1.630, P 0.05). The serum levels of calcium and osteoealine in high fluoride group were (1.13±0.27)mmol/L and (6.56±5.74)μg/L, respectively, which were lower than in the control group[ (1.82±0.37)mmol/L and (23.45±15.40)laeJL, respectively], but the levels were elevated to (1.76±0.36)mmol/L and (10.57±4.28)μg/L when high fluoride was combined with low aluminum, and further elevated to (2.10±0.51)mmol/L and (15.73±3.15)μg/L when high fluoride was combined with high aluminum. The urinary calcium level in low fluoride group [ (6.24±2.61)retool/retool Cr] was higher than that in the control group[ (3.12±2.04)retool/retool Cr], but it was decreased in low fluoride and aluminum groups[ (0.81±0.44), (1.23± 0.41)mmol/mmoi Cr, respectively]. On the other hand, the levels of serum ealeium and osteocaline in high aluminum group were (1.07±0.68)mmol/L and (7.21±5.22)μg/L, elevated to (1.47±0.18)mmol/L and (10.98±4.35) μg/L when low fluoride was combined wth high aluminum, and further elevated to (2.10±0.51)mmol/L and (15.73± 3.15)μg/L when high fluoride was.combined with high aluminum, respectively, and the combined effects showed the same trend of higher aluminum. Conclusions Aluminum antagonized fluoride-induced effects, whereas fluoride aggravated the effects caused by aluminum in this experimental conditions. The biomarkers of bone formation and mineralization were suppressed in the combined groups, so the combined effects could interfere with the course of bone turnover by inhabiting bone formation and mineralization, leading to the disorder of bone metabolism eventually.

Objective To investigate the combined effects of fluoride and aluminum intoxication on bones and their possible mechanisms.Methods Kunming mice were divided into nine groups according to the factorial experiment design.Different dose of fluoride(NaF,0,50,150 mg/L)and/or aluminum(AlCl3,0,200,600 mg/L)was administered to each group in drinking water.After 24 weeks,the degree of mottled teeth and the histomorphometric parameters,such as the bone trabecula and osteoid areas,the number of osteoblasts and osteoclasts,and pathologic changes in femur were observed.Results Aluminum could also caused mottled teeth(in degree 4).The mottled teeth in the combined groups were more serious than those in fluoride or aluminum alone group.The interaction between fluoride and aluminum existed in the changes of bone trabecula and osteoid areas(F=2.963,3.688,P＜0.05),and not existed in changes of the number of osteoblasts and osteoclasts(F=2.347,0.888,P＞0.05).In high fluoride group,the trabecula and osteoid areas were(50 675.47±22 916.34),(10 733.97 ±3015.55)μm2,but it increased to(75 988.64±13 797.21),(16 402.88±4605.83)μm2 when combined with high aluminum(P＜0.05),and the group of high fluoride +low aluminum increased to(69 277.16±19 837.51),(18 564.79±6362.47)μm2 (P＜0.05),so aluminum antagonized the effects induced by fluoride;the area of bone trabecula of group of high aluminum was(60 718.43 ±17 574.37)μm2,but it increased[(75 988.64±13 797.21),(82 474.94±15 466.66)μm2]when combined with high or low fluoride(P＜0.05),and the combined effects showed a similarity to those in high aluminum group.The prominent osteoporosis with increased osteoid and cartilage tissues,and decreased amount of bony matrix and minerals were the main histopathological changes in the bone.Conclusions Both high aluminum and fluoride intoxication can result in mottled teeth,their combined effects are more serious than the individual effect.The prominent injury of combined fluoride and aluminum intoxication is osteomalacia and osteoporosis.