The relationship between hydrogen sulfide （H2S） and nitric oxide （NO） in myocardial infarction （MI） has not been previously reported. In the current investigation, we sought to determine the roles of both H2S and NO in MI in rats. Animals were randomly divided into 5 groups and treated with L-NG-nitro arginine methyl ester （L-NAME）, sildenafil, saline, propargylglycine （PAG） and L-cysteine, respectively, for 1 week prior to performing MI surgery or sham operation. The mortality rates were lower in sildenafil and L-cysteine treated rats in the MI group. The infarct area was significantly reduced in sildenafil and L-cysteine treated rats. Moreover, plasma H2S measurements revealed that the level in the sildenafil treated group was lower than in the L-NAME treated MI group, which was consistent with an observed decrease in cystathionine gamma-lyase （CSE） enzyme activity. CSE protein expression level in the L-NAME treated MI group was significantly higher than in sildenafil treated MI group. eNOS protein content in the L-cysteine treated MI group was lower than in the PAG treated MI group and eNOS gene expression is significantly decreased in the L-cysteine treated rats. We demonstrated that endogenous H2S and NO are cardioprotective in the rat model of MI. Indeed, both the H2S-CSE and NO-NOS system appear to have a mutual down-regulation effect in MI process in our experimental rat model.
Atrial fibrillation （AF） remains one of the leading causes of morbidity and mortality in the world which are related to palpita- tions, fainting, congestive heart failure or stroke. The mechanism for atria/fibrillation has been identified as electrical remod- eling, structure remodeling and intracellular calcium handling remodeling, microRNAs （miRNAs） have recently emerged as one of the important factors in regulating gene expression. So far, thousands of miRNA genes have been found in diverse ani- mals with the function of regulating cell death, cell proliferation, haematopoiesis and even participate in the processing of car- diovascular disease. In this review, we summarize the mechanism of AF and the association of microRNAs network with AF. We provide a potential perspective of miRNAs as the therapeutic target for AF.
MicroRNAs(miRNAs)are endogenous small non-coding RNA molecules that posttranscriptionally regulate gene expression.MiRNA expression and function in heart disease remain to be determined but modulation of miRNA expression in vivo has revealed that miRNAs play an important role in controlling heart function and structure.In fact,abnormal expression of miRNAs may initiate and contribute to the progress of heart disease.Here,we summarize the literature relating to the involvement of miRNAs in cardiac hypertrophy,myocardial fibrosis and heart failure.
Objective To assess the anti-arrhythmic activity and cardioprotective effects of Wenxin Granula,a traditional Chinese formula(consisting of Salviae Miltiorrhizae Radix,Polygonati Rhizoma,Notoginseng Radix et Rhizoma,Nardostachyos Radix et Rhizoma,Angelicae Sinensis Radix,and Succinum),on heart in ischemic-induced myocardial infarction(MI) rats and compare with those of Amiodarone which have been demonstrated in clinic.Methods Rats were randomly divided into Sham-operated(control),MI + Amiodarone [5 mg/(kg.d)](MI),and MI + Wenxin Granula [10 mg/(kg.d)] groups and left anterior descending coronary artery was occluded in each group.After left anterior descending for 12 h,standard lead II of administration electrocardiogram was recorded in order to analyze the occurrence of arrhythmia.After one month,the size of the infarct area of heart was evaluated by TTC staining method and haemodynamic function was assessed to detect the heart function.Laser scanning confocal microscope and the technique of patch clamp were used to detect the intracellular Ca2+([Ca2+]i) and L-type calcium current(ICa-L),respectively.Results Both Wenxin Granula [10 mg/(kg.d)] and Amiodarone [5 mg/(kg.d)] could markedly decrease the incidence of arrhythmia in heart of rats which were subjected to ischemic injury.After one month,Wenxin Granula could significantly decrease mortality to 22.22% and reduce the infarct area(P < 0.05),but Amiodarone did not.The mechanism may involve that Wenxin Granula attenuated [Ca2+]i decreasing in MI rats.Additionally,Wenxin Granula could obviously ameliorate the impaired heart function of MI rats by decreasing the elevated left ventricular end-diastolic pressure and increasing the attenuated maximum change velocity of left ventricular pressure in the isovolumic contraction or relaxation period.On the other hand,electrophysiological experiment results revealed that Wenxin Granula administration one month later also increased the reduced ICa-L density in rat ventricular myocytes in MI rats.The results of LSCM showed t
LI Xiao-xue1,LI Xue-lian1,CHU Wen-feng1,2,CAI Rui-jun1,SHI Yong-fang1,XU Chao-qian1,2,SHAN Hong-li1,2,WANG Xing-yang1,LU Yan-jie1,2,YANG Bao-feng1,2 1.Department of Pharmacology,Harbin Medical University,Harbin 150081,China 2.The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China,Key Laboratory of Cardiovascular Research,Ministry of Education,Harbin Medical University,Harbin 150081,China
Previous studies have demonstrated the important role of taurine in inhibiting proliferation of myofibrob lasts（myoFb） and myocardial fibrosis. However, the underlying mechanisms are unclear. The present study was de signed to shed light on this issue through exploring the signal pathways via in vitro experiments. Angiotension II （AngII） treatment significantly increased myoFb proliferation and the levels of collagens I and III（P〈0.05）, whereas taurine, PKCα（PKC： protein kinase C） specific inhibitor L-threo-dihydro-sphingosine（D4681）, ERK1/2 inhibitor （PD98095） abrogated myoFb proliferation and collagen levels（P〈0.05, P〈0.01, respectively）, and increased the G0/G1 phase rate and decreased S phase rate. Immunocytochemistry, confocal fluorescence staining and image analy sis showed that taurine could inhibit the translocation and expression of p-PKCαin membrane, and then inhibit nuc lear translocation and expression of p-ERK1/2. These results have statistically significant differences compared with those of AngII group（P〈0.01）. Western blot results also show that taurine could inhibit the protein expression of p-PKCα and p-ERK1/2. We used p-PKCα specific inhibitor D4681 in order to elucidate the relationship between p-PKCα and p-ERK1/2 in signal transduction pathways. Finally, the results show that the protein expression of p-ERK1/2 and nuclear translocation were suppressed in D4681 group.
WANG Li-ying1,2, LI Hong1 and YANG Shi-jie1 1. Department of Pharmacology, Norman Bethune College of Medicine, Jilin University, Changchun 130021, P. R. China
