Aim The present study focused on the changes of leukocyte adhesion to endothelial cells and the effects of sasanquasaponin(SQS) on these changes. Methods After pretreated by SQS (10.0, 1.0, 0.1 ?mol?L~(-1)) for 5 hous, human umbilical vein endothelial cells (HUVECs) were exposed to heat-stress for 3 hours. Lactate dehydrogenase (LDH) activity in the HUVECs supernatants was determined. The resulting HUVECs viability and leukocyte adhesion rate were measured spectrophotometrically. The expression of ICAM-1 was assayed by western blots. Results Elevation of LDH activity, enhancement of leukocyte adhesion rate and ICAM-1 expression level were observed in heat-stress group, and there were significant differences compared with control group (P

AIM: To study protective effects as myocardial ischemic preconditioning of sasanquasaponin (SQS) and its relationship with K ATP channel. METHODS: The study adopted the model of myocardial ischemic injury induced by subcutaneous injection of isoproterenol (ISO) in rats, administering specific K ATP channel blocker gliberclamide (GLI 5 mg?kg -1 ). Four groups were set as NS group, I/R group, SQS group ( 0.2 mg?kg -1 ), and GLI group (5 mg?kg -1 ). Prior to injection of ISO, all agents were intraveneously injected into rats for 3 days, one time per day. Subsequently, ISO was subcutaneuously injected into rats by the ways of many different sites, and some indices were measured including ECG, serum creatine kinase (CK) activity, free fatty acid (FFA), and adenosine contents in rats. RESULTS: Preconditioningly intravenous injection of SQS could effectively protect myocardium from ischemic injury induced by ISO. With GLI injected prior to SQS, the cardioprotective effects of SQS were significantly attenuated. CONCLUSION: SQS can protect myocardium from ischemic injury induced by ISO, and the protection may be mediated by K ATP channel.

AIM In this study, we observe the effects of SQS on contents of myocardial malondialdehyde(MDA)and activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH Px) through adopting the model of myocardial ischemic injury induced by subcutaneous injection of isoprenaline(ISO 4 mg?kg -1 ?d -1 ?2 d) into rats. METHODS Four groups were divided, namely NS, I/R, SQS1 and SQS2 group. The contents of MDA and activities of SOD and GSH Px were examined after administering SQS for 3 days(1 time per day). RESULTS The results show the elevation of S T in ECG, increase of MDA contents and decrease of SOD and GSH Px activities in I/R group. SQS may antagonize the changes of MDA, SOD and GSH Px induced by ISO, revealing the relationship to dose dependence. CONCLUSION SQS is most likely to possess the capabilities of anti oxygen free radicals and anti lipoperoxidation to myocardial ischemic injury induced by ISO.

Object To study the protective effect and pharmacological ischemic preconditioning of sasanquasaponin (SQS) on intact rat heart and its relationship with NO Methods A model of rat myocardial ischemia induced by sc injection of isoproterenol (ISO) was prepared, and after the administration of selective NO synthesis inhibitor methylene blue (MET), the ECG, serum creatine kinase (CK) activity, free fatty acid (FFA) and adenosine contents were determined Results Preconditioning iv injection of SQS can effectively protect the myocardium from ischemia induced by ISO The cardio protective effect was significantly attenuated when the NO synthesis inhibitor MET were injected prior to SQS Conclusion SQS can effectively protect myocardium ischemia induced by ISO and the protection is most likely to be mediated by NO

Objective To investigate the effect of sasanquasaponin (SQS) on injury of endothelial cells induced by hypoxia-reoxygenation and neutrophil adhesion, and its possible mechanisms. Methods Human umbilical vein endothelial cells (HUVEC) were exposed to normoxia or hypoxia-reoxygenation in the absence or presence of SQS (10.0, 1.0, and 0.1 ?mol/L). Lactate dehydrogenase (LDH) activity was determined in cultured HUVEC supernatants. HUVEC survival rate, neutrophil adhesion rate, malondialdehyde (MDA) level superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured. Neutrophil adhesion was assayed in additional HUVEC treated as above. Results The results showed that hypoxia-reoxygenation resulted in HUVEC injury and enhancement of neutrophil adhesion, with the increase in LDH activity, MDA level, and adhesion rate as well, conversely, with the decrease in activity of SOD and GSH-Px; SQS antagonized these changes in a concentration-dependent manner. Conclusion SQS may protect HUVEC against hypoxia-reoxygenation injury and its mechanism appeares to be related to anti-lipoperoxidization and anti-adhesion of white blood cell.

Objective To explore the application effect of simethicone combined with compound polyethylene glycol electrolyte powder before colonoscope examination. Methods 106 cases underwent colonoscope examination from October 2013 to December 2015 were enrolled in the study. Then all the cases were divided into 2 groups randomly, each with 53 cases. Patients in the control group were treated with simple oral administration of compound polyethylene glycol electrolyte powder, patients in observation group were combined using simethicone and polyethylene glycol electrolyte powder. The preoperative bowel preparation score, lesion detection and the changes of liver and renal function and electrolyte in the two groups were recorded respectively. Results Patients in the observation group were better than the control group in both the bowel preparation score and the detection rate (P < 0.05). There were no obvious adverse reactions in the course of the two groups. Conclusions Simethicone can eliminate intestinal bubbles, and combined use with polyethylene glycol electrolyte powder before colonoscope examination can significantly improve intestinal cleaning effect, improve the colonoscope examination image, enhance the detection rate of lesions.

Aim To investigate the role of captopril in insulin resistance of endothelial cells induced by high glucose.Methods 1 .Improvement effect of captopril on insulin resistance in HUVECs was observed.The HUVECs were seeded in a 6-well plate and were ran-domly divided into 5 groups,namely,control group, IR group,IR together with different Cap concentrations (low,medium and high concentration),respectively. 2.Improvement effect of Cap on insulin resistance was mediated by PPARγin HUVECs.HUVECs were ran-domly divided into 6 groups,namely,control group, control +PPARγinhibitor (PI)(1 .0 μmol · L -1 ) group,IR group,IR +PI(1 .0 μmol·L -1 )group,IR +Cap(1 ×1 0 -5 mol·L -1 ) group,and IR +Cap +PI (1 .0 μmol·L -1 )group.All indicators were detected. Results After HUVECs were incubated with media containing 33 mmol·L -1 of glucose for 48 h,the NO levels were significantly decreased while ET-1 levels were significantly elevated,showing a significant differ-ence between IR group and control group (P <0.01 ). The expression levels of PPARγmRNA and its protein were somewhat up-regulated,but there was no signifi-cant difference between IR group and control group (P>0.05).When the HUVECs in IR group were treated with DMEM containing glucose (33 mmol·L -1 )for 48 h and insulin for 30 min,the expression levels of PPARγmRNA and its protein in Cap groups were simi-lar to those in the IR group,and there was no signifi-cant difference between the two groups (P >0.05 );however, the expression levels of phosphorylated PPARγprotein in Cap groups were increased compared with IR group (P <0.05).The levels of NO were sig-nificantly increased whereas the levels of ET-1 were decreased in Cap groups,which had significant differ-ences compared with IR group (P <0.05).Nonethe-less,pre-treating with GW9662,a PPARγinhibitor, the improvement effects of Cap were markedly abol-ished.Conclusions Captopril could improve high glucose-induced insulin resistance of endothelial cells mediated by PPARγ,and the underlying mechanisms are related to the activation of PPARγ,rather than its expression.

[ ABSTRACT] AIM:To investigate the protective effect of naringin ( Nar) on the injury of human umbilical vein endothelial cells ( HUVECs) induced by 33 mmol/L high glucose ( HG) and to explore its possible mechanisms.METH-ODS:The injury model was established by treating HUVECs with HG medium for the indicated time (6, 12, 24, 48 and 72 h) , and then the levels of NO, eNOS and p-eNOS were detected, respectively.The effects of Nar on high glucose-in-duced endothelial cell injury were observed.HUVECs were treated with Nar at concentrations of 5, 10, 25, 50 and 100 mg/L for 6 h, 12 h, 24 h, 36 h and 48 h.The levels of NO in the supernatants were measured.The effects of Nar on HG-injured HUVECs were explored by treating the cells with 10 μmol/L of LY294002, a PI3K inhibitor, or 0.5 μmol/L of AKT inhibitorⅣ, an AKT inhibitor, and then the levels of NO, PI3K, AKT, eNOS and their phosphorylated proteins were determined by Western blot.RESULTS:Nar at concentration of 50 mg/L significantly attenuated the injury of endothelial cells induced by high glucose ( P<0.01) , and the protective effects of Nar were abolished by pretreating with the inhibitor of PI3K or AKT (P<0.01).CONCLUSION: Nar protects endothelial cells against the injury induced by high glucose through PI3K/AKT/eNOS pathway.

Objective To investigate the association of estrogen receptor-? (ER-?) and vitamin D receptor (VDR) gene polymorphisms with peak bone mass in Shanghai women. Methods The ER-? PvuⅡ and XbaⅠ genotypes and VDR ApaⅠ genotypes were determined by PCR-RFLP in 515 unrelated healthy women aged 19-40 years of Han nationality in Shanghai. Bone mineral density (BMD) was measured by dual-energy X-ray absorptiometry. Results Frequencies of ER-? PvuⅡ genotype PP, Pp and pp were 13.2%, 49.3% and 37.5% respectively. Frequencies of ER-? XbaⅠ genotype XX, Xx and xx were 4.7%, 40.4% and 54.9% respectively. Frequencies of VDR ApaⅠ genotype AA, Aa and aa were 5.8%, 41.9% and 52.3% respectively. Hardy-Weinberg equilibrium was evident for both ER-? and VDR gene polymorphisms. No association was found between ER-? PvuⅡ and XbaⅠ genotypes and BMD of various sites in women. Only a significant association was found between VDR ApaⅠ genotype and BMD at L 1-4(P

BACKGROUND: Peak bone mass and standard deviation (SD) in different regions are varied, which have great influence on diagnosis of osteoporosis. To establish a complete database can provide accurate evidence for osteoporosis diagnosis. OBJECTIVE: To investigate the influence of bone mineral densities (BMD) and their SD of young people on the detective rate of osteoporosis in general population. DESIGN, TIME AND SETTING: Investigation analysis was performed at Beijing, Shanghai, Guangzhou, Nanjing, Jiaxing and Chengdu between January 1997 and December 1999. PARTICIPANTS: 11418 subjects from related 6 centers of BMD reference database in China were investigated and analyzed using prospective and retrospective methods, including 3 666 males, and 7 752 females aged 20-90 years. Of them, 2385 were from Beijing, 1178 from Guangzhou, 1404 from Shanghai, 2938 from Nanjing, 1425 from Chengdu, and 2088 from Jiaxing. The subjects were selected from community investigation, physical examination volunteers. METHODS: BMD of the lumbar spine (L2-4) and the hip in 11, 418 subjects from the related 6 centers in China was measured with GE-Lunar dual energy X-ray absorptiometry (DXA) and the BMD reference database was established. The accuracy rate of the inner machine was 0.3%-0.7%, and the accuracy of different machines averaged 1.1%. MAIN OUTCOME MEASURES: Lumbar BMD distribution of different age groups from 6 centers; influence of young people's BMD and its SD on detective rate of osteoporosis. RESULTS: Different BMD and SD were found in the individual subject from 6 centers, and the maximum differences were 0.098 g/cm2 and 0.027 g/cm2. With mean BMD and SD of the individuals from 6 centers as references, different T-scores and the detective rates of osteoporosis derived from the T-scores were found in the same group. The detective rate increased by 1.6% when BMD of the young people increased by 0.01 g/cm2 (positive correlation), but the detective rate decreased by 4% when SD increased by 0.01g/cm2 (negative correlation). CONCLUSION: Changes in BMD and SD of the young people can influence the detective rate of osteoporosis. To achieve comparability for the detective rate of osteoporosis in different centers, the specific reference database should be established for the same race, the same area, and the same bone densitometry machine. The T-score should be determined with the normal BMD and SD of the young, people as the reference database.