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The Effect of TanshinoneⅡ A upon the TGF-beta1/Smads Signaling Pathway in Hypertrophic Myocardium of Hypertensive Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第4期29卷 476-480页

作者：李永胜杨宇平于丹梁黔生 Department of Emergency Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Pharmacology School of PharmacyXinxiang Medical University

To investigate the molecular mechanism by which Tanshinone Ⅱ A （TSN Ⅱ A） prevents left ventricular hypertrophy （LVH）, we examined the expression of AT1R, TGF-β1 and Smads gene in the hypertrophic myocardium of hypertensive rats with abdominal aorta constriction. LVH model was established by creating abdominal aorta constriction. Four weeks later, animals were randomly divided into 4 groups with 8 animals in each. One group was used as model control, the other three groups were treated with TSN ⅡA （20 mg/kg）, TSN ⅡA （10 mg/kg） and valsartan （10 mg/kg）, respectively. Another 8 SD rats were subjected to sham surgery and served as blank control. After 8- week treatment, the caudal artery pressure of the animals was measured. The tissues of left ventricle were taken for the measurement of the left ventricular mass index （LVMI） and pathological sectioning and HE-staining were used for determining the myocardial fiber dimension （MFD）. The mRNA expression of AT1R, protein expression of TGF-betal and activity of Smad-2, 4, 7 were detected by RT-PCR and Western blotting, respectively. Our results showed that （1） the blood pressure of rats treated with TSN Ⅱ A, either at high or low dose, was significantly higher than those in the control and valsartan-treated group （P〈0.01, P〈0.05）; （2） LVMI and MFD in TSN Ⅱ A and valsartan-treated rats were higher than those in the control group （P〈0.05） but significantly lower than those in the model control （P〈0.01）; （3） the high doses of TSN Ⅱ A and valsartan significantly down-regulated the mRNA expression of AT 1R and protein expression of TGF-beta l and Smad-3 in the hypertrophic myocardium （P〈0.01）, and TGF-betal in valsartan-treated animals was more significantly lower than that in rats treated with TSN Ⅱ A; （4） the two doses of TSN Ⅱ A and valsartan significantly up-regulated the protein expression of Smad-7 in the hypertrophic myocardium （P〈0.01）, and Smad-7 in the animals treated with high-dose TSN Ⅱ A was significantly higher tha

关键词： Tanshinone ⅡA pressure overloading myocardial hypertrophy AT1R TGF-betal Smads

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Magnolol attenuates right ventricular hypertrophy and fibrosis in hypoxia-induced pulmonary arterial hypertensive rats through inhibition of the JAK2/STAT3 signaling pathway

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中国药理学与毒理学杂志 2021年第10期35卷 763-764页

作者： FU Min-yi LUO Fang-mei WANG E-li JIANG Yue-ping LIU Shao LUO Xiu-ju PENG Jun LIU Bin Department of Pharmacy Xiangya HospitalCentral South UniversityChangsha 410008China Department of Pharmacy Hunan Children′s HospitalChangsha 410007China Department of Pharmacology Xiangya School of Pharmaceutical SciencesCentral South UniversityChangsha 410078China Department of Laboratory Medicine The Third Xiangya HospitalCentral South UniversityChangsha 410013China Hunan Provincial Key Laboratory of Cardiovascular Research Xiangya School of Pharmaceutical SciencesCentral South UniversityChangsha 410078China

OBJECTIVE Right ventricular(RV)remodeling is one of the essential pathological features in pulmonary arterial hypertension(PAH).RV hypertrophy or fibrosis are the leading causes of RV *** is a compound isolated from Magnolia *** possesses multiple pharmacological activities,such as anti-oxidation and *** study aims to evaluate the effects and underlying mechanisms of magnolol on RV remodeling in hypoxia-induced ***①Male SD rats(220 g)were randomly divided into 5 groups(n=10):the normoxia group,the hypoxia group,the hypoxia plus Magnolol(10 and 20 mg·kg^(-1)·d-1)group,and the vehicle *** in the normoxia group were kept in a normoxia environment for 4 weeks,while rats in the hypoxia group were kept in a hypoxic chamber(10%O2).The rats in the hypoxia plus magnolol groups were administered with magnolol at 10 or 20 mg·kg^(-1)(ip)once a day for 4 *** the end of 4 weeks,the heart function was assessed by Doppler echocardiography,and then the rats were anesthetized with sodium pentobarbital(30 mg·kg^(-1),ip).The RVSP was measured by the right heart catheterization *** heart tissues were collected and dissected to calculate the index of RV remodeling(RV/LV+IVS,RV/tibial length,or RV/body weight).Part of the RV samples was fixed with 4%paraformaldehyde for morphological analysis,while other samples were frozen at-80℃for molecular studies(measurements of ANP,BNP,α-SMA,and collagenⅠ/ⅢmRNA expression as well as p-JAK2/JAK2 and p-STAT3/STAT3 protein levels).②To evaluate the effect of magnolol on hypoxia-induced myocardial hypertrophy and fibrosis,H9c2 or cardiac fibroblasts were divided into 7 groups:the control group,cells were cultured under normal conditions;the hypoxia group,cells were cultured under hypoxic condition(3%O2);the hypoxia plus magnolol 10 mg·kg^(-1) group,magnolol10μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus magnolol 30 mg·kg^(-1) group,magnolo

关键词： magnolol right ventricle remodeling myocardial hypertrophy myocardial fibrosis JAK2 STAT3

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Effects of transforming growth factor-β_1 and signal protein Smad3 on rat cardiomyocyte hypertrophy

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Chinese Medical Journal 2004年第10期117卷 1471-1475页

作者：黄俊覃国辉胡昌兴龚丽娅程芳舟马业新陆再英 Department of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Cardiology First Affiliated Hospital Jiangxi Medical College Nanchang 330006 China Department of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Background SMAD proteins have recently been identified as the first family of putative transforming growth factor-β_1(TGF-β_1) signal transducers. This study was to investigate the effects of TGF-β_1 and signal protein Smad3 on rat cardiac *** The incorporation of [3H]-leucine was measured to determine the hypertrophy of cardiomyocyte incubated with different doses of TGF-β_1 in cultured neonatal cardiomyocytes. The model of rat cardiac hypertrophy was produced with constriction of the abdominal aorta. At different times after the operation, rats were killed, and their left ventricular mass index (LVMI) determined. The mRNA expression of TGF-β_1 and Smad3 of cultured cells and hypertrophic left ventricles were assessed by RT-PCR. The protein expression of Smad3 was assessed by Western *** In cultured neonatal cardiomyocytes, TGF-β_1 significantly promoted incorporation of [3H]-leucine. With the concentration of 3 pg/L, it increased the expression of Smad3 in mRNA and protein levels after 15 minutes, and continued for up to 8 hours of cultured cardiomyocytes. The LVMI and the expression of TGF-β_1 (mRNA) and Smad3 (mRNA and protein) of hypertrophic left ventricle were increased by day 3 after the operation and continued to the 4th week. The peak expression of these was in the second week after *** TGF-β_1 has positive effects on rat cardiomyocyte hypertrophy. Signal protein Smad3 could be related to the pathologic progression of rat cardiac hypertrophy.

关键词： TGF-β_1 myocardial hypertrophy signal protein Smad3

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Inhibitory Effect of Sodium Ferulate on the Cardiomyocyte hypertrophy Induced by AngiotensionⅡ

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神经药理学报 2017年第3期7卷 57-58页

作者： LUO Min CHEN Pan-pan YANG Lu SHI Jing-shan DENG Jiang Key Laboratory of Bisic Pharmacology of Ministry of Education School of pharmaceutical science Zunyi Medical University

Objective:To investigate the effects of sodium ferulate（SF） on myocardial hypertrophy of rat and explore the protective mechanism. Methods:The myocardial hypertrophy was induced by 0.1 μmol·L;Ang II. The cytoactive was detected by MTT. The cultured cardiomyocytes from Sprague Dawley neonate rats were randomly divided into normal,model,L-arginine(L-arg 1 000 μmol·L;) group and SF(50,100,200 μmol·L;) *** observe whether SF had nonspecific injurious effect on the cells,SF 200 μmol·L;was added into the normal cardiomyocytes and to determine whether the effect of SF on cardiomyocyte hypertrophy was associated with NO release,another two groups were established. NG-nitro-L-arginine-methyl ester（L-NAME） 1 500 μmol·L;combined with SF 200 μmol·L;or L-arg 1 000 μmol·L;,respectively. Cardiomyocyte hypertrophy was confirmed by observing the histological changes and the measurements of cell diameter,protein content and ANF and β-MHC m RNA expression of the *** levels of NO,NOS and eNOS activity,the contents of cGMP and cAMP. The expression of eNOS were detected by Real time PCR and Western blotting. Results:（1） SF(50,100,200 μmol·L;) had no obvious side effect on cultured neonatal rat cardiomyocytes in vitro. In the group added 0.1 μmol·L;Ang Ⅱ alone,the cells displayed swollen,with undistinguishable border;the diameter and protein content of cardiomyocytes was increased remarkably,and the expression of ANF and β-MHC m RNA were up-regulated by Ang Ⅱ. SF and L-arg could ameliorate the cardiomyocyte hypertrophy which can be inhibit by L-NAME.（2） Compared with normal group,0.1 μmol · L;Ang II could decrease the NO content,NOS and eNOS activity in supernatant of cultured cardiomyocytes,decrease the content of cGMP and increase the content of cAMP incardiomyocytes,upregulation the expression of ***-H and L-arg administrated could siginificantly ameliorate these changes. Conclusion:SF can inhibit cardiomyocyte hypertrophy induced Ang Ⅱ in rats. The probable mechanism in

关键词： sodium ferulate myocardial hypertrophy angiotensin Ⅱ nitric oxide cyclic guanosine phosphate

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Sodium ferulate inhibits cardiomyocyte hypertrophy induced by Ang Ⅱ through enhancement of NO/cGMP signaling pathway

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中国药理学与毒理学杂志 2019年第10期 796-796页

作者： CHEN Pan-pan LUO Min LU Yan-liu JIN Feng GONG Qi-hai SHI Jing-shan DENG Jiang Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education Zunyi Medical University The First People′ s Hospital of Zunyi and The Third Affiliated Hospital of Zunyi Medical University

OBJECTIVE The present study is to investigate the effect of SF on neonatal rat cardiomyocytes of myocardial hypertrophy induced by 0.1 μmol · L;angiotensinⅡ（AngⅡ） and explore the underlying *** The cultured cardiomyocytes from Sprague Dawley neonate rats were randomly divided into: normal,model(AngⅡ0.1 μmol·L;), L-arginine(1000 μmol·L;)group and SF(50, 100, 200 μmol·L;) group. To observe whether SF had nonspecific injurious effect on the cells,SF 200 μmol·L;was added into the normal cardiomyocytes. To determine whether the effect of SF on cardiomyocyte hypertrophy is associated with NO release, another two groups[NG-nitro-L-arginine-methyl ester（L-NAME）]1500 μmol·L;combined with SF 200 μmol·L;and L-arginine 1000 μmol·L;) were established. RESULTS After administration, Ang Ⅱ decreased the NO content, NOS and e NOS activity in supernatant of cultured cardiomyocytes, and decreased the content of c GMP and increased the content of c AMP in cardiomyocytes, up-regulation the expression of PKC-β, Raf-1, ERK1/2 and down-regulated the expression of MKP-1 and e NOS. SF 200 μmol·L;and L-argininesignificantly ameliorated these *** ameliorate the cardiomyocyte hypertrophy which can be inhibited by L-NAME. These results indicate that SF can inhibit cardiomyocyte hypertrophy induced by AngⅡand the probable mechanism involved to promote NO/c GMP signaling pathway and inhibit PKC and MAPK signaling pathway. CONCLUSION These results indicate that SF can inhibit cardiomyocyte hypertrophy induced by AngⅡ and the probable mechanism involved to promote NO/c GMP signaling pathway and inhibit PKC and MAPK signaling pathway.

关键词： sodium ferulate myocardial hypertrophy angiotensin Ⅱ nitric oxide protein kinase C mitogen activated protein kinase

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