Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups：cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments，the expression of PCNA, NOS and the cell number was tested, respectively.Results：After treated with Losartan，the cell number of group 2 was(4.17±0.15)×105，the OD value of PCNA was 0.202 6±0.007 6，both of which were less than that of cells of group 3；the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) (P＜0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.

AIM: To observe the effect of angiotensinⅡ subtype 2 receptor (AT_2 receptor) on the cultured rat aortic vascular smooth muscle cells. METHODS: The plasmid contained the cDNA of AT_2 receptor was transfected into cultured rat vascular smooth muscle cells. The effects of AngⅡ, Ang Ⅱ+losartan, Ang Ⅱ+PD123319 on the expression of PCNA, the NOS activity and the cell number were observed. RESULTS: The cell number and the expression of PCNA decreased after the cells were treated with losartan. When treated with PD123319, the cell number and the expression of PCNA increased, but the expression of NOS decreased. CONCLUSIONS: These data suggest that when being activated, AT_2 receptor inhibits the proliferation of vascular smooth muscle cells and antagonizes the effect of AT_1 receptor, such an effect may be related to the activation of NOS. [

AIM: To study the effect of thyroid hormone on the expressional change of myosin heavy chain(MHC) gene in cardiomyocyte induced by angiotensinⅡ(AngⅡ) and its potential mechanism. METHODS: Cardiac myocyte was cultured according to the method of Simpson. 10 -8 mol/L T_3 and 10 -7 mol/L AngⅡ were added to the culture medium,respectively or synchronously. After 48 h,the expression of ? and ?-MHC mRNA in myocytes were detected by RT-PCR. The protein kinase C activation were detected by PepTag non-radioactive PKC assay. The incorporation of -Leucine and -thymine to test the protein and DNA synthesis in myocytes were also performed. RESULTS: AngⅡalone increased the incorporation of -Leucine of myocytes while it had no effect on the incorporation of -thy mine. The expression of ?-MHC mRNA was increased and the expression of ?-MHC mRNA was decreased significantly at the condition of AngⅡ. The enhanced PKC activation was induced by AngⅡalso. When AngⅡand T_3 were added to the culture medium synchronously,though the incorporation of -leucine and -thymine were not changed compared with AngⅡ treated alone. The ?-MHC mRNA expression was increased and the ?-MHC mRNA expression was decreased significantly. The PKC activation of the myocytes also was decreased. CONCLUSIONS: T_3 inhibited the expressional change of myosin heavy chain gene in cardiac myocytes induced by AngⅡ. The effect of T_3 on the change of PKC activation in cardiac myocytes may be one of its mechanisms.

This article deals with the influence of shear stress on endothelial NO synthesis, and the role of caveolae in shear stress-induced eNOS activation. Human umbilical vascular endothelial cells (HUVEC) were cultured and exposed to different levels of laminal shear stress and Filipin, the perfused cultures were collected, and NO(2-)/NO(3-) was detected using nitrate reduction method. The structure of caveolae was observed through transmission electron microscopy (TEM). The level of NO(2-)-/NO(3-) was found to increase with the elevation of shear stress level (P < 0.01). It was the highest at 1.5 N/m2. After treatment with Filipin, the level of NO produced by HUVEC decreased significantly (P < 0.01), but after recovery and shear without Filipin, the level of NO synthesis bounded back (P < 0.01). It was then concluded that shear stress can induce endothelial NO synthesis and caveolae plays a key role in shear stress-induced eNOS activation.
Caveolae ; physiology ; Cells, Cultured ; Endothelium, Vascular ; cytology ; Filipin ; pharmacology ; Humans ; Nitric Oxide Synthase Type III ; metabolism ; Shear Strength ; Umbilical Veins ; cytology

Objective To explore the effects of ischemia and ischemia reperfusion on the proliferation,apoptosis,migration ability,inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) expression of endothelial progenitor cells (EPCs).Methods Collection of peripheral blood from volunteers and culture of endothelial progenitor cells in vitro.The cells were divided into three groups:control group,hypoxia group and hypoxia reoxygenation group.Methyl thiazolyl tetrazolium (MTT) assay was used to detect cell proliferation.Transwell chamber method was used to detect cell migration.Cell apoptosis was detected by flow cytometry.Western blot was used to detect iNOS and eNOS expressions.Results A confocal microscope was used to observe the basic adherence of the cells to the wall for about 3 days,and the area became larger.After 7 d of single nucleus cell culture,the growth of colony-like pattern was more than that of spindle.The cell counts of the three groups in the microscope were (1.83 ± 0.92),(5.07± 0.84),(2.11 ± 0.74).Compared with the control group (0.24 ± 0.04),the hypoxia group (0.62± 0.06) could promote EPCs proliferation,and the difference was statistically significant (t =12.142,P ＜ 0.05);While there was no significant difference between the hypoxia reoxygenation group (0.39 ± 0.06) and the control group (P ＞ 0.05).The number of cell migration in the hypoxia group (18.28 ± 2.05) and hypoxic complex oxygen group (14.08 ± 2.11) was not statistically significant compared with the control group (15.14 ± 1.25) (P ＞ 0.05).The apoptosis rate in hypoxia group (34.57 ±0.42)％ and hypoxia reoxygenation group (41.08 ± 0.44)％ was significantly higher than that in control group (24.83 ± 0.38) ％ (x2 =13.427,15.084,P ＜ 0.05).The apoptosis rate of hypoxia reoxygenation group was significantly higher than that of hypoxia group (x2 =9.657,P ＜ 0.05).The expression of iNOS in hypoxia group and hypoxia reoxygenation group was significantly higher than that in control group,and the difference was statistically significant (P ＜ 0.05).Conclusions Ischemia could promote the proliferation of EPCs,and increase the expression of iNOS,but the expression of EPCs was down-regulated after reperfusion.

Objective:To investigate the effect of hydroxysafflor yellow A(HSYA) preconditioning group on apoptosis induced by cold hypoxia/reoxygenation (cold H/R) injury in human renal tubular epithelial cells (HK2 cells).Methods:After digestion and passage, HK2 cell lines were divided into Sham group (control group), cold hypoxia and reoxygenation group (cold H/R group, cells cold hypoxia for 4 h, reoxygenation for 4 h), and HSYA preconditioning group (each HSYA subgroup was given different doses of HSYA 0.5 h before hypoxia, and the other operations were the same as the cold H/R group). The cell survival rate was measured by CCK-8 method.The expression of Bcl-2, Bax and Caspase-3 proteins in HK-2 cells were detected by immunocytochemistry and Western blotting.Results:(1) Compared with cold H/R group, different doses of HSYA could improve cell survival rate in different degrees, but only HSYA25 μmol/L group had the most significant effect (74.000±5.500 vs.59.000±3.800, P<0.05). (2) Immunocytochemistry semi-quantitative score: Compared with cold H/R group, the expression of Bax and Caspase-3 in HK2 cells of HSYA25 μmol/L group was significantly decreased(0(0, 1) vs. 8(6, 8), Z=2.041, P<0.05 and (3.400±0.548) vs.(7.800±1.095), t=11.000, P<0.01). The expression of Bcl-2 protein was increased significantly ((6.800±1.095) vs.(1.400±0.548), t=10.590, P<0.01). The ratio of Bcl-2/Bax increased significantly.(3)Western blot was used to detect protein: Compared with the cold H/R group, the protein levels of Bax, Cleaved-Caspase-3 and Pro-caspase-3 of HK2 cells in the HSYA25 μmol/L group were significantly decreased ((0.707±0.012) vs.(0.968±0.117), (0.480±0.009)vs.(0.735±0.005), (0.992±0.008)vs.(1.197±0.005), all P<0.01). The expression of Bcl-2 protein was significantly increased, and the ratio of Bcl-2/Bax was significantly increased ((0.410±0.009) vs.(0.273±0.008), (0.582±0.016) vs (0.282±0.080), all P<0.01). The experimental results were consistent with the immunocytochemistry. Conclusion:HSYA can effectively reduce the damage of HK2 cells after cold hypoxia and reoxygenation.

Objective To investigate the efficacy and safety of Irbesartan Hydrochlorothiazide combined with Metoprolol as initial therapy in the treatment of heart failure in the elderly.Methods A total of 128 elderly patients with heart failure admitted into our hospital from September 2017 to August 2018 were randomly divided into Group A(n=64)and Group B(n=64).Group A was treated with oral Irbesartan Hydrochlorothiazide tablets.Group B was treated with sustained-release oral Metoprolol tablets in addition to what was given in Group A.Therapeutic effects were compared between the groups.Results Compared with Group A,the effectiveness rate of group B was significantly improved(93.8％ vs.81.3％,x2 =4.571,P=0.033).There was no significant difference in brain natriuretic peptide (BNP),interleukin (IL)-12,left ventricular ejection fraction (LVEF),left ventricular end-systolic diameter(LVESD),or left ventricular end-diastolic diameter(LVEDD)between the two groups before treatment (P＞0.05).Compared with Group B,BNP,IL-12,LVEF,LVESD and LVEDD had significantly better profiles in Group A after treatment (P ＜ 0.05).The time-domain measurements of heart rate variability such as sequential five-minute R-R interval means(SDANN),standard deviation of the N-N interval(SDNN),percent of differences between adjacent RR intervals ＞50ms(PNN50)and root mean square of the successive differences(RMSSD)were higher in Group B than in Group A after treatment.No serious adverse reactions were observed in either group,and there was no significant difference in the incidence of adverse reactions between the two groups(4.7％ vs.7.8 ％,x2 =0.533,P =0.465).Conclusions Irbesartan Hydrochlorothiazide combined with Metoprolol as initial therapy has good clinical effects in treating elderly heart failure.It can not only improve the clinical symptoms of patients,but also ensure clinical medication safety.

Objective To explore the effect of different types of helicobacter pylori(Hp)on carotid atherosclerosis(CAS)and the efficacy of rosuvastatin.Methods Totally 346 subjects were examined in the physical examination center of our hospital from February 2020 to June 2022.According to the results of 14C urea breath test and Hp antibody typing,they were divided into 102 cases of type Ⅰ Hp infection group,79 cases of type Ⅱ Hp infection group and 165 cases of Hp negative group,inflammatory factors,blood lipids and carotid artery ultrasound were also examined.All subjects with carotid atherosclerosis were instructed to treat with rosuvastatin 10mg/d,and the level of low density lipoprotein cholesterol(LDL-C)was rechecked after 4 weeks.Results There were significant differences in high sensitivity C-reactive protein(hs-CRP),IL-6 and tumor necrosis factor-α(TNF-α)between the three groups(P<0.05).Compared with Hp negative group,cholesterol(TC)and LDL-C in type Ⅰ and type Ⅱ Hp infection groups were significantly increased,while high density lipoprotein cholesterol(HDL-C)in type Ⅰ Hp infection group was significantly decreased;compared with type Ⅱ Hp infection group,LDL-C in type Ⅰ Hp infection group was significantly increased,and HDL-C was significantly decreased(P<0.05).The detection rate of stable plaque and unstable plaque in Hp positive subjects was significantly higher than that in Hp negative subjects(P<0.05);the detection rate of stable plaque and unstable plaque in type Ⅰ Hp infected subjects was significantly higher than that in type Ⅱ Hp infected subjects(P<0.05);after adjusting for age,hypertension,diabetes and other risk factors,it was still an independent risk factor of carotid atherosclerotic plaque vulnerability.After 4 weeks,the LDL-C level of CAS subjects in the three groups before and after treatment was significantly different(P<0.05).Compared with the type Ⅰ Hp group,the LDL-C level of CAS subjects in the Hp-negative group was significantly lower(P<0.05).Conclusion Hp infection,especially type Ⅰ Hp infection,is related to dyslipidemia,stimulation of inflammatory reaction and instability of carotid plaque,affecting the efficacy of lipid-lowering drugs.

Objective To understand the current situation of health education contents as well as the differences in their requirements between clinical medical students and clinicians,and to provide reference for the optimization of health education curricula for medical students.Methods A stratified sampling method was adopted to select 511 medical students (303 females and 208 males) from a medical university,and the survey results of 436 clinicians (144 females and 292 males) were taken as reference.Differences in the degrees of need between clinical medical students and clinicians were compared by chi-square tests.Results There were statistical differences in needs between clinical medical students and clinicians regarding drug compliance,smoking cessation intervention,balanced diet,application of Chinese traditional rehabilitation medicine,mobile health technology education,exercise rehabilitation guidance,and theory of health promotion (P＜0.01).With regard to drug compliance,smoking cessation intervention,and exercise rehabilitation guidance,the proportions of clinical medical students' needs were just 87.1％,82.2％,and 81.2％,respectively,but for clinicians the proportions reached up to 96.3％,93.8％,and 92.8％,respectively.Whereas,there were no statistical differences for mental stress management,chronic infectious disease health education,and acute infectious disease health education (P＞0.05).Conclusion There is still a big gap between medical students and clinical doctors when it comes to the knowledge of chronic disease management and healthy lifestyles;clinical medical students have not yet realized the importance of such knowledge and skills.Therefore,the strengthening of course construction for clinical medical students is suggested.

Objective To investigate the role of triggering receptor expressed on myeloid cells-1(TREM-1)in ath-erosclerosis induced by chronic intermittent hypoxia(CIH).Methods ApoE-/-mice were randomly divided into blank group,model group and experimental group.The mice in the model group and the experimental group were kept in a hypoxic environment and fed with a high-fat diet.After 4 weeks of high-fat feeding,mice in the experi-mental group were intraperitoneally injected with TREM-1 inhibitor LR12(5 mg/kg)for 8 weeks.After 12 weeks of feeding,the level of serum total cholesterol(TC),low density lipoprotein(LDL),triglyceride(TG),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-10(IL-10)were detected.Histological analysis of aortic TREM-1 expression,plaque area and macrophage level were examined.Results Compared with blank group,the expression of TREM-1 in the aorta of the model group significantly increased(P＜0.05).Com-pared with model group,the aortic plaque,the level of lipids in serum(TC,LDL,TG)and inflammatory factors(TNF-α,IL-1β,IL-10),aortic plaque,the expression of TREM-1 and infiltrating macrophages in aortic plaque of the experimental group were all significantly reduced(P＜0.05).Conclusions TREM-1 is involved in the develop-ment of CIH-induced AS.Inhibition of TREM-1 can alleviate CIH-induced AS and its mechanism is related to the inhibition of macrophage activation.