Aim To investigate the effects of angiotensin-converting enzyme inhibitor Ena on proliferation and cell cycle protein of cardiac fibroblasts and to explore the mechanism of Ena on cardiac fibrosis.Methods CFb was isolated by trypsin digestion method.MTT colorimetric assay was adopted to evaluate cell proliferation,collagen synthesis was observed by hydroxyproline concentration method,flow cytometry,immunofluorescenic and Western blot was used to measure cell cycle and CKI p27kip1 with Ena.Results Ena decreased MTT value and collagen synthesis dramatically;Ena increased phase G0/G1 and decreased phase S percentage ratio in cell cycle;Ena enhanced p27kip1 protein expression in a dose-dependent manner.Conclusion The antiproliferative effects of Ena on CFb can be attributed to upregulating CKI p27kip1 protein expression.

Objective To study the relationship with internet addiction disorder(IAD)of the youth,the degree of IAD and home environment,attachment.To study the relationship with home environment and attachment.Methods 490 students were assessed with Internet Addiction Disorder Test,FES-CV,Attachment Questionnaire.Results 37 subjects can be defined as IAD according to Internet Addition Disorder test;IAD group have a higher score in contradictoriness(P＜0.05)of home environment and lack of maternal love,lack of fatherly love,father's rejection,parent's passive entangle,angry with parent[the average score of IAD group Was 13.16±4.62,14.18±5.42,14.41±5.44,19.10±4.59,18.89±4.42,12.37±4.80,11.35±4.17;the average score of normal group was 11.77±4.06,11.59±4.02,16.56±4.99,15.78±4.91,9.87±4.52,9.65±4.25,P＜0.05,0.01].Home environment were significantly correlated with all factors of attachment except independence(P＜0.05,0.01).There Was a significant negative correlation between the degree of IAD and lack of maternal love(r=-0.360).Conclusion Contradiction in home environment and passive attachment,that played an important role in internet addiction disorder of the youth.

Objective To investigate the anti-proliferation effect of Ginseng Rh2(G-Rh2)on mouse MFC gastric cells and its mechanism.Methods MFC cells (1.0?109?L-1) were divided into four gourps:control group and G-Rh2(3,10,30 mg?L-1) groups.The cell viability was determined by MTT;the cell cycle was detected by flow cytometry;the protein expression of cyclin D1 and p27kip1 were observed respectively by qualitative and quantitative analysis.Results Compared with control group,the cell viabilities decreased gradually with the increasing of dose and time in G-Rh2(3,10,30 mg?L-1) groups at different time(1,2,4 h)(P

Aim To investigate the effects of enalapril(Ena) on cardiac fibrosis induced by isoprenaline(Iso) and to explore its mechanism.Methods Effect of Ena and captopril(Cap) on collagen content,HW/BW,LVI,hydroxyprolnie(Hyp) level,and TGF-?1 protein expression was observed with IH and WB in rats induced by Iso subcutaneous injection.Results Different doses of Ena could decrease HW/BW,LVI and Hyp level dramatically,and decrease TGF-?1 protein expression which was closely related to myocardial fibrosis(MF).Conclusion Enalapril can inhibit TGF-?1 protein expression,by which inhibit myocardial fibrosis.

A dynamic model of disease can be used to quantitatively describe the pattern and characteristics of disease transmission, predict the disease status and evaluate the efficacy of control strategy.This review summarizes the basic transmission dynamic models of echinococcosis granulosus and their application.

Objective To observe the effects of ACE inhibitor enalaprilat(Ena) and protein kinase C(PKC) inhibitor chelerythrine(Chele)on proliferation,collagen Ⅰ,cell cycle,PKC and cyclinD1 protein expression of neonatal cardiac fibroblasts(CFb) and to probe its molecular mechanism.Methods CFb of neonatal Wistar rats were divided into control group,AngⅡ group,Chele+AngⅡ group,Chele+AngⅡ+Ena group and AngⅡ+Ena group.CFb were isolated by trypsin digestion method.MTT colorimetric assay was adopted to evaluate cell proliferation,immunocytochemical staining(IC) was used to measure collagen Ⅰ content,Western blotting and flow cytometry were used to detect PKC,cyclinD1 and cell cycle respectively.Results Compared with AngⅡ group,the MTT value decreased dramatically(P

Myocardial fibrosis is the common results of the development of a variety of heart diseases which leads to extracellular matrix protein metabolic disorders and causes cardiac remodeling owing to cardiac fibroblasts proliferation, eventually results in malignant arrhythmia, heart failure, and even the occurrence of sudden cardiac death. Effective inhibition of myocardial remodeling could prevent the occurrence of sudden death. To know the protein kinase C (PKC) effective mechanism of regulation on myocardial fibrosis, a new therapeutic target for reversing myocardial remodeling might be provided.

AIM To investigate the effect of urapidil on NO, ET, ANF and AngⅡ of spontaneously hypertensive rats. METHODS The content of nitric oxide (NO), endothelin (ET), atrial natriuretic factor (ANF) and angiotensin Ⅱ (AngⅡ) were determined by spectrophotometry and radioimmunoassay of spontaneously hypertensive rat (SHR) during the process of decreasing blood pressure with urapidil. RESULTS\ They were as follows: compared with the same aged normal blood pressure WKY rats, in the SHR, the content of serum NO decreased, the level of ET and ANF in the plasma increased. Whereas the level of AngⅡ has no difference in any group. Compared with the control of SHR,urapidil can increase the contents of serum NO, decrease the level of ET and ANF in the plasma. CONCLUSION \ It is suggested that urapidil may adjust the imbalance of cardiovasco-active substances by increasing the release of endogenous vasodilators and reducing the release of endogenous vasocontrictors to antihypertention.

Aim To investigate the effect of taurine(Tau)on the cardiac fibroblast(CFb)cell cycle and its regulatory protein expression,and to explore the underlying mechanism of Tau-inhibiting the proliferation of CFb.Methods The proliferation of cultured neonatal rat CFb was induced by Angiotensin Ⅱ and detected by the thiazole blue(MTT)colorimetric assay.Hydroxyproline measurement was carried out to detect the collagen quantification.The expression of cell cycle regulatory protein cyclin D and p27 were determined by the combination of immunocytochemical staining and image analysis software.Cell cycle and p27 were assessed via flow cytometry.Results CFb proliferation and hydroxyproline content in culture medium were markedly inhibited when CFb were treated with taurine at concentrations of 40,80 and 160 mmol?L-1 for 24 hours(P

Aim To investigate the molecular mechanism of anti-proliferation effect of Ginsenoside Rh2(G-Rh2)on mouse MFC gastric cells.Methods The cell viability was determined by MTT method and the state of cell proliferation was analyzed.The morphologic changes were observed by invert microscope and fluorescence microscope(Hoechst 33258).Early apoptotic rate was detected by Annexin Ⅴ-FITC through flow cytometry.Western blot was used to detect the p-JNK and p-c-jun activity in MFC cells.Immunocytochemistry staining was used to detect caspase-3 positive cells.Results G-Rh2 could inhibit proliferation of MFC cells in a dose-and-time-dependent manner.The morphological changes of apoptosis were observed in MFC cells after G-Rh2 treatment.The apoptotic ratio was increased.The phosphorylation of c-Jun and c-Jun NH2-terminal kinase(JNK)activity increased with time within 4 h compared with that of control.The expression of caspase-3 positive cells was increased.But all the above could be partly inhibited by pre-treatment with SP600125(5 ?mol?L-1)for 2 h.Conclusion G-Rh2 can decrease cell viability by inducing apoptosis and the process may be associated with the activation of JNK transduction pathway and expression of caspase-3.