Objectives To explore the clinical effect of coupling meglumine cyclic adenylate (MCA)and the human granulocyte colony-ostimulating factor (G-CSF)on rat with diastolic heart failure(DHF).Methods Totally 60 rats of DHF model were evenly divided into 4 groups according to random number:Control group(n=15,control),Model group(n=15,DHF model),MCA group(n =15,treated with MCA)and MCA+GCSF group(n=15,treated with MCA plus G-CSF).MCA group were administered by intragastric injection of MCA 30 mg/kg/d for 15 d,MCA+G-CSF group were administered by intragastric injection of MCA 30 mg/kg/d and plus G-CSF 100 μg/kg/d for 15 d,while Control group and Model group were given same volume of saline solution.BIOPAC SYSTEM was used to analyze the model establishment.The mRNA levels of GATA-4 and Cx43 were measured by RT-PCR.The protein expressions of GATA-4,Cx43,cTNI and c-kit were measured with western blotting.ELISA and flow cytometry were used to detect cAMP and differentiation rate of bone marrow mesenchymal stem cells (BMSCs),respectively.Results Compared with MCA group,the denaturation degree of myocardial tissues in DHF rat was significantly improved than in MCA+G-CSF group.Moreover,the level of GATA-4 (1.62 ± 0.09),Cx43 (1.02 ± 0.07),cTNI (1.42 ± 0.12),c-kit (0.65±0.02),cAMP(283.67± 18.09)nmol/L and BMSCs cell differentiation rate(38.62 ± 1.52)％ in MCA + GCSF group were significantly promoted (all P＜ 0.05)than in MCA group,GATA-4 (0.82±0.07),Cx43 (0.52±0.05),cTNI(0.86 ± 0.13),c-kit (0.48 ± 0.03),cAMP(198.83 ± 16.03) nmol/L and BMSCs cell differentiation rate (19.82 ± 0.89)％.Conclusions The combination of MCA with G-CSF is significantly improved DHF than single MAC treatment,which may regulate BMSCs differentiation though cAMP/PKA signaling pathways.

Objective To observe whether recent sexual intercourse might cause microscopic hematuria, and investigate the cause of hematuria. Methods Eighty healthy volunteers (40 men and 40 women) consented to have intercourse with their married couples and provide samples of urine for testing before intercourse and the first day morning, noon, evening and the second day morning after intercourse. After appropriate instruction, volunteers tested their own urine for the presence of blood using standard dipsticks. Any volunteer with hematuria after intercourse was offered a comprehensive hematuria assessment and followed-up for two years. Results None of the volunteers had positive hematuria before sexual intercourse. 9 of the 40 women, but no men, had positive hematuria at the first day morning after intercourse, and 3 of the nine patients with hematuria still had positive hematuria at the noon of the first day. Five women of 9 patients with hematuria accepted two years follow-up and no abnormal was identified. Conclusion It suggested that recent sexual intercourse was a cause of asymptomatic microscopic hematuria in women, and a history of recent sexual intercourse should be considered when assessing the clinical significance of microscopic hematuria in women.

Objective To investigate the relationship between the plasma levels of ET-1,TAT,and hs-CRP and slow coronary flow syndrome (SCFS),and explore effects of coronary endothelial function,coagulation function,and inflammatory reaction on blood flow of coronary artery.Methods A total of 400 cases with normal blood flow of coronary artery by coronary angiogram was randomly selected.The coronary flow patterns were determined by corrected thrombolysis in myocardial infarction frame count method (cT-FC).Among them,45 cases whose average cTFC more than 27 were assigned as SCFS group,the other 45 cases no SCFS.Plasma levels of ET-1,TAT and hs-CRPwere examined with enzyme-linked immunosorbent assay (ELISA),and were compared between two groups.Moreover,multivariate analysis evaluating predictors of SCFS was performed with regression test.Results No statistical difference was found between two groups concerning the gender,history of hypertension,diabetes mellitus,and cigarette alcohol percentage..The plasma level of HDL in SCFS group was lower than that of no SCFS [(1.22 ± 0.42) mmol/L vs (1.44±0.34) mmol/L,t =-2.731,P ＜0.01],but the plasma level of glucose in the former was higher than that of the latter [(5.68 ±0.62) mmol/L vs (5.10 ±0.84) mmol/L,t =3.727,P ＜0.01].However,Plasma levels of ET-1,TAT and hs-CRP in SCFS were higher than that of no SCFS [(94.3 ± 16.78) ng/Lvs (83.5±12.53) ng/L,t =3.051,P ＜0.01;(12.96±3.24)μg/Lvs (8.76 ±2.64)μg/L,t =5.945,P ＜ 0.01 ; (2.48 ± 0.35) μg/L vs (1.38 ± 0.46) μg/L,t =11.259,P ＜ 0.01].Furthermore,Logistic regression analysis showed that ET-1,TAT and hs-CRP were risk factors for SCFS (OR ＞ 1.22).Conclusions Due to coronary endothelial dysfunction,endothelial inflammatory reaction,and activated coagulation function,slow coronary flow of coronary artery occurs.

Objective To investigate the prevention and mechanism of Extracorporeal shock wave lithotripsy(ESW) induced renal Injury by pre-treating kidneys with low-energy shock waves(LESW).Methods Forty healthy female domestic rabbits were surgically managed to the mono-nephron models and random divided into 4 groups consisting of ten each: Control,LESW,ESW and ESWL plus LESW pretreated groups.LESW group received 100 LESW,ESW group received 1500 standard ESW,and same dose on ESW group except 100 LESW pretreatment in ESW plus LESW pretreated group.The rabbit kidney tissues were obtained 24 hours after ESW.Activity of superoxide dismutase(SOD) and malondialdehyde(MDA) levels in the renal tissue,and the level of N-acetyl-β-D-glucosaminidase(NAG) in urinary were measured.Renal cell apoptosis was detected by TdT-mediated dUTP Nick End Labelling(TUNEL).Results The MDA,the urinary level of NAG and rate of apoptosis in the LESW groups were reduced(P<0.01),and the activity of SOD increased significantly(P<0.05) as compared with ESW group,and these changes in LESW group had no statistics difference compared with the control group(P>0.05).Conclusions LESW pretreatment protocol substantially limits the renal injury that often caused by ESW.LESW may suppress oxidative stress and antagonize the process of renal cellular apoptosis.

Objective: To study the impact of astragaloside on ventricular remodeling and peroxisome proliferator activated receptor a (PPARa) expression in pressure-overload rats and to preliminarily explore its mechanism. Methods: Pressure-overload rat's model was established by abdominal aorta constriction (AAC) in 8-week old SD rats and the result was conifrmed by echocardiography at 6 weeks later. Pressure-overload rats were divided into 4 groups with different intragastric treatment: Model control (normal saline) group, Benazepril hydrochloride [10mg/(kg.d)] group, Low-dose astragaloside [40mg/(kg·d)] group and High-dose astragaloside [80mg/(kg.d)] group; in addition, Sham operation group, the rats received intragastricnormal normal saline.n=20 in each group and all animals were treated for 8 weeks. Rat's cardiac structure and function indexes were assessed by echocardiography, hemodynamic parameter was examined by left ventricular intubation, myocardium and blood levels of free fatty acid (FFA) were determined, morphological changes of myocardial tissue was observed by HE and Masson staining, mRNA and protein expressions of PPARa were measured by qRT-PCR and Western blot analysis. Results: Compared with Sham operation group, Model control group showed increased left ventricular mass index(LVMI), collagen volume fraction (CVF) and FFA level, allP<0.05, while decreased mRNA and protein expressions of PPARa, bothP<0.05. Compared with Model control group, Low-dose and High-dose astragaloside groups presented reduced LVMI, CVF and FFA level, allP<0.05-0.01, while elevated mRNA and protein expressions of PPARa, bothP<0.01. Conclusion:Astragaloside IV mayinhibit myocardial remodeling in pressure-overload rats, which might be via up-regulating mRNA and protein expressions of PPARa, enhance myocardiumFFA utilization, and therefore improve myocardial energy metabolism.

Objective: To observe the effects of astragaloside IV on myocardial fibrosis and connective tissue growth factor (CTGF) expression in experimental rats with chronic heart failure (CHF).
Methods: CHF model was established by abdominal aorta constriction (AAC) and the rats were divided into 5 groups:Sham operation group, the rats received normal saline 2 ml/day, n=10, CHF group, the rats received normal saline 2 ml/day, n=12;Astragaloside IV groups, CHF rats received astragaloside IV at (20, 40, 60) mg/kg respectively and n=12 in each group. All animals were treated for 4 weeks. Hemodynamic indexes were monitored, left ventricular mass index (LVMI) was calculated, morphologic changes of myocardial tissue was observed by HE staining, myocardial ifbrosis degree and collagen volume fraction (CVF) were measured by Masson staining. The mRNA and protein expressions of CTGF were detected by RT-PCR and immunohistochemistry, Western-blot analysis respectivety.
Results: Compared with CHF group, 3 Astragaloside IV groups had decreased LVMI and CVF, P<0.05-0.01;Astragaloside IV (40 and 60) mg/kg groups presented decreased LVEDP and LVSP, increased ±dp/dtmax, P<0.01 to P<0.05 and improved pathological morphology. Compared with Sham group, CHF group had increased average CTGF OD value (0.09 ± 0.03) vs (0.45 ± 0.04) and increased expression of myocardial CTGF (0.57 ± 0.06);compared with CHF group, the average CTGF OD values in Astragaloside IV (20, 40, 60) mg/kg groups were all decreased (0.39 ± 0.05), (0.30 ± 0.06), (0.24 ± 0.04) and decreased expressions of myocardial CTGF (0.44 ± 0.05), (0.35 ± 0.02), (0.28 ± 0.03) respectively, all P<0.01.
Conclusion: Astragaloside IV can inhibit myocardial ifbrosis and improve cardiac function in CHF rats, which might be via inhibiting the over expression of myocardial CTGF.

AIM:To observe the effects of astragaloside IV (AS-IV) on myocardial fibrosis in chronic heart failure ( CHF) rats and to explore the underlying mechanism preliminarily .METHODS:Chronic heart failure model rats established by abdominal aorta constriction (AAC) were divided into CHF group, valsartan group and AS-IV group.Sham operation group was also established .The rats in valsartan group and AS-IV group received valsartan and AS-IV at 2 and 30 mg· kg-1 · d-1 , respectively.The rats in sham operation group and CHF group received normal saline .After 8 weeks of treatment, the cardiac structure and the hemodynamic parameters were measured .The morphologic changes of myocardial tissue were observed after staining .The expression of long-chain acyl-CoA dehydrogenase ( LCAD) and 6-phosphofructoki-nase-1 (PFK1) at mRNA and protein levels was determined by RT-qPCR and Western blot.RESULTS:Compared with sham operation group , left ventricular mass index ( LVMI) , collagen volume fraction ( CVF) , left ventricular posterior wall depth (LVPWD), and the mRNA and protein of PFK1 in CHF group were increased (P<0.05), while the mRNA and protein levels of LCAD were decreased (P<0.05).Compared with CHF group, the LVMI, CVF, LVPWD, and the mRNA and protein levels of PFK1 in valsartan group and AS-IV group were decreased (P<0.05), while the mRNA and protein levels of LCAD were increased (P<0.05).CONCLUSION:AS-IV inhibits myocardial fibrosis in the CHF rats , the mechanism of which might be associated with up-regulating the expression of LCAD , down-regulating the expression of PFK1 and normalizing the myocardial energy metabolism .

Ventricular myocytes from hearts of the neonatal SD rats were treated with 10-7,10-6,and 10-5 mol/L simvastatin for 72 hours under high glucose condition. Compared with control group,the viability of cadiomyocyte was significantly lower in high glucose group (P＜0.01 ).The activity of lactate dehydrogenase,the relative expressions of NADPH oxidase subunits p22phox,p47phox mRNA,and reactive oxygen species level in the high glucose group were higher than those of control group ( all P＜0.05).lndexes mentioned above were significantly improved by simvastatin treatment in a dose-dependent manner.These results suggest that simvastatin ameliorates high glucose-induced injury of cardiomyocytes via increasing the expression of NADPH oxidase mRNA.

Objective:To investigate the effect of Astragaloside Ⅳ on high glucose-induced cardiomyocyte pyroptosis.Methods:H9c2 cells were cultured in vitro and divided into control group(5.5 mmol/L glucose), high glucose group(33.3 mmol/L glucose), Astragaloside Ⅳ group(33.3 mmol/L glucose+ 100μmol/L Astragaloside Ⅳ), and NLRP3 inhibitor group(33.3 mmol/L glucose+ 1μmol/L MCC950). Cell counting kit 8(CCK-8)was used to detect the activity of H9c2 cells.Lactate dehydrogenase(LDH)kit was used to detect the content of LDH in cell supernatant.Superoxide anion fluorescent probe(DHE)was used to detect the level of intracellular reactive oxygen species(ROS). Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and Western blot were used to detect the mRNA and protein expression levels of pyroptosis-related genes.Immunofluorescence was used to detect the fluorescence intensity of NLRP3.Enzyme-linked immunosorbent assay(ELISA)was used to detect the level of inflammatory factors in cell supernatant.Results:When the concentration of Astragaloside Ⅳ was 100 μmol/L, it could significantly inhibit the decrease of cardiomyocyte viability induced by high glucose( P<0.01)and reduce LDH release( P<0.01). Compared with the control group, the level of ROS was increased( P<0.01), the mRNA and protein expressions of pyroptosis-related molecules were up-regulated( P<0.01 for all), the fluorescence intensity of NLRP3 was increased( P<0.01), and the levels of inflammatory factors in the cell supernatant were increased in the high glucose group( P<0.01). Compared with the high glucose group, the ROS level was decreased( P<0.01), the mRNA and protein expressions of pyroptosis-related molecules were down-regulated( P<0.05 or P<0.01), the fluorescence intensity of NLRP3 was decreased( P<0.01), and the levels of inflammatory factors in cell supernatant were decreased( P<0.05 or P<0.01)in Astragaloside Ⅳ group and inhibitor group. Conclusions:Astragaloside Ⅳ plays a protective role in high glucose-induced cardiomyocyte injury by inhibiting NLRP3/Caspase-1 signaling pathway and inhibiting pyroptosis.Moreover, it can improve the anti-inflammatory and antioxidant properties in cell models.

Objective To analyze changes in serum levels of inflammatory factors,galectin-3 (Gal-3),fractalkine(FKN) and interleukin-6 (IL-6),in patients with dilated cardiomyopathy (DCM) or ischemic cardiomyopathy (ICM),and to explore their clinical significance.Methods Seventy-six hospitalized patients with DCM were selected to serve as a DCM group,and 78 patients with ischemic cardiomyopathy were selected into an ICM group from October 2016 to December 2017 at the Department of Cardiology,and patients in the two groups received cardiac function classification.Meanwhile,82 healthy people were included as a control group.Fasting venous blood was collected,and serum levels of Gal-3,FKN,IL-6,and BNP were measured.The correlations of Gal-3,FKN,and IL-6 with DCM or ICM were analyzed.Results Levels of plasma BNP and serum Gal-3,FKN,and IL-6 in the DCM and ICM groups were higher than those in the control group,and their levels in the DCM group were significantly higher than in the ICM group.Levels of plasma BNP and serum Gal-3,FKN,and IL-6 increased as their New York Heart Association(NYHA)classification went higher in both the DCM and ICM groups.For patients classified at the same level,serum levels of Gal-3,FKN,and IL-6 of the DCM group were significantly higher than those of the ICM group(P ＜ 0.05).BNP levels showed no difference between the two groups(P ＞0.05).Spearman correlation analysis indicated positive correlations of NYHA classification with levels of BNP(r =0.30,0.19),Gal-3(r=0.24,0.19),FKN(r =0.63,0.51),and IL-6(r =0.28,0.15)in both the DCM and ICM groups(P ＜ 0.05),and the correlation was stronger in the DCM group.Conclusions Increased expression of plasma BNP,Gal-3,FKN,and IL-6 in patients with DCM and ICM are closely related to the severity of cardiac function impairment.Monitoring changes in levels of plasma BNP and serum inflammatory factors Gal-3,FKN and IL-6 provides important clues for the differential diagnosis between DCM and ICM,the assessment of clinical conditions and treatment-related decisions.