ABSTRACT
Objective To observe the protective effect of meicha protein on the heart of spontaneously hypertensive rats(SHR),and explore its mechanism.Methods Fourty healthy SHR rats were randomly divided into 4 groups:model control group,Meicha protein low dose group(70 mg·kg-1)、Meicha protein high dose group(140 mg·kg-1),Compound Kendir Leaves Tablets group(50 mg·kg-1),n=10.The rats were orally administered twice daily by gavage for seven weeks,measuring blood pressure in each group fort nightly.1 h after the last administration,drawing off the blood from carotid,stripping off the heart tissue,and the organ index was calculated;Taking a part of the tissue with 4% paraformaldehyde for Pathological histology.Detection of serum NO,ET-1 levels as well as the organization of the ACE and Ang II mRNA expression to explore the mechanism of its buck.Results Meicha protein could significantly reduce the blood pressure of SHR;The impact on the rat organ coefficient was not obvious,but had a protective effect on heart tissue.Compared with the model control group,the contents of NO an ET-1 were significantly increased(P<0.01).Compared with the model group,the high dose of Meicha protein could induce ACE,AngⅡ,CYP11B2.The expression of mRNA was significantly decreased(P<0.01).Conclusion The possible mechanism of Meicha protein antihypertensionis relevant to increase the content of NO in serum,reduce the content of ET-1 in serum,reduce mRNA expression of ACE and AngⅡin cardiac tissue.
ABSTRACT
Objective To investigate the effect of mycophenolic acid (MPA) on the endotheline-1 (ET-1) induced proliferation, contraction and migration of pulmonary arterial smooth muscle cells (PASMCs)and to explore the mechanism of MPA on pulmonary arterial hypertension (PAH), and the effect of exogenous guanosine nucleotide reversing anti-proliferative effect of MPA. Paired-samples t-test was used for statistical analysis. Methods MTT test, scarification test, Millicell cell culture insertion and the length of PASMCs mcasured under microscope were used. Results The A values of group ET-1 + low concentration MPA decreased when compared with group ET-1 (0.348±0.036 vs 0.447±0.013, t=6.357, P=0.000) and the A values of group ET-1 + high concentration MPA was further decreased. The A values of group ET-1 + low concentration MPA + guanosine was higher than that of group ET-1 + low concentration MPA (0.390±0.018 vs 0.348 ±0.036, t=2.573, P=0.028). The average migration distance and the average migration numbers of PASMCs of groups MPA was decreased than that of group ET-1. The average cell length of PASMCs of groups MPA was increas ed than that of group ET-1. Conclusion MPA can effectively inhibit the proliferation,contraction and migration of PASMCs by ET-1 induction. The IMPDH may play a role in anti-proliferative effect of MPA on PASMCs, but is unnecessary to be the sole mechanism. These findings has provide new insight into the mechanisms of mycophenolate mofetil in the treatment of PAH.
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Objective To study the influence of Nictinamide on the endotheline(ET-1)in patienta with pulmonary arterial hypertension(PAH).Methods 66 cases of PAH were divided randomly into two groups (n=33for each):the Nictinamide treatment group and the control group.The changes of endotheline were compared before and after treatment.Results After treatment serum endotheline was significantly lower in the treatment group(P＜0.01),but there was no difference in the control group before and aftertreatment(P＞0.05).The significant difference was observed between treatment group and control group(P＜0.01).Conclusion Nictinamide will reduce the level of endothellne and confers some degree therapeutic and preventive value for PAH.
ABSTRACT
PURPOSE: Mycoplasma pneumoniae frequently causes lower respiratory illnesses in children, and is known to be associated with acute wheezing and the exacerbation of asthma. However, the mechanism by which this pathogen contributes to the development of wheeze- related symptoms is not fully understood. Previous studies have shown that ET-1 is a potent bronchoconstrictor and implicated in the pathogenesis of bronchial asthma. The aim of our study was to examine the serum ET-1 and other cytokines in M. pneumoniae pneumonia and investigate if there is any difference in relation to the presence of wheezing. METHODS: Patients admitted with pneumonia were divided into three groups: M. pneumoniae pneumonia with wheeze (group 1) and without wheeze (group 2), and patients with pneumonia due to other pathogens (group 3). The serum levels of ET-1, IL-18, IL-5 were measured by ELISA in patient groups and controls. RESULTS: Serum ET-1 increased significantly in the patients with M. pneumoniae pneumonia (groups 1 and 2) compared with group 3 and controls. ET-1 in group 1 was significantly higher than in group 2. IL-5 and IL-18 were higher in patient groups than in controls with no difference between groups. Serum total IgE was significantly higher in group 1 than in group 2. A positive correlation was observed between serum ET-1 and total IgE. CONCLUSION: Our results suggest that ET-1 may be implicated in the pathogenesis of bronchoconstriction and allergic inflammation in the airways of the patients with M. pneumoniae pneumonia.