Volume 35 Issue 2
Mar.  2019
Turn off MathJax
Article Contents
YUANLu, LIANGBo-zhi, LUOJian-hua, LULi-na, YANGHui, LILi, YANGDong-hua. Effect and Mechanism of Leonurine on Rats with Ventricular Remodeling Induced by Isoproterenol[J]. Journal of Nanjing University of traditional Chinese Medicine, 2019, 35(2): 180-184.
Citation: YUANLu, LIANGBo-zhi, LUOJian-hua, LULi-na, YANGHui, LILi, YANGDong-hua. Effect and Mechanism of Leonurine on Rats with Ventricular Remodeling Induced by Isoproterenol[J]. Journal of Nanjing University of traditional Chinese Medicine, 2019, 35(2): 180-184.

Effect and Mechanism of Leonurine on Rats with Ventricular Remodeling Induced by Isoproterenol

  • Publish Date: 2019-03-10
  • OBJECTIVE To observe the effect of leonurine on rats with ventricular remodeling induced by isoproterenol(ISO) and to explore the possible mechanism involved. METHODS SD rats (n=10) were used as normal control group, and 80 rats were given ISO by intraperitoneal injection daily for 2 weeks to establish the model of ventricular remodeling. The model rats were divided into 5 groups randomly as model group, low-dose leonurine (7.5 mg/(kg·d)) group, middle-dose leonurine (15 mg/(kg·d)) group, high-dose leonurine (30 mg/(kg·d)) group and p38MAPK inhibitor (0.3 mg/(kg·d)) group. After the treatment for 2 weeks, the pathological change of left ventricular myocardial tissues was observed by HE staining,and the expression of TGF-β1 was determined by the method of immunohistochemistry. The serum concentrations of ET-1 and NO were measured by ELISA and nitrate reductase methods, respectively. The expression of p38MAPK, MEF2,β-MHC and α-MHC mRNA was detected by qPCR, and the protein expression of ET-1, p-p38MAPK and MEF2 was determined by Western blot. RESULTS Compared with model group, the pathological change of ventricular remodeling in high-dose leonurine group was attenuated, and the serum concentrations of NO and the mRNA expression of α-MHC in left ventricular myocardial tissues of high-dose leonurine group were higher (P<0.05).The expression of TGF-β1, the serum concentrations of ET-1, the mRNA expression of p38MAPK,MEF2 and β-MHC mRNA, and the protein expression of ET-1, p-p38MAPK and MEF2 were lower than those in model group (P<0.05). CONCLUSION Leonurine attenuates ventricular remodeling in the rats induced by ISO, and it is potentially associated with inhibiting p38MAPK/MEF2 signaling pathway.

     

  • loading
  • [1]
    AZEVEDO PS, POLEGATO BF, MINICUCCI MF, et al. Cardiac remodeling: Concepts, clinical impact, pathophysiological mechanisms and pharmacologic treatment[J]. Arq Bras Cardiol, 2016,106(1): 62-69.
    [2]
    ZHU YZ, WU W, ZHU Q, et al. Discovery of Leonuri and therapeutical applications: From bench to bedside[J].Pharmacol Ther, 2018, 188:26-35.
    [3]
    梁赵文,罗建华,杨冬花,等.益母草碱对慢性心力衰竭心肌重构大鼠心房利钠肽、血管紧张素Ⅱ影响的研究[J].贵州医药,2016,40(12):1235-1238.
    [4]
    NGUYEN MN, KIRIAZIS H, GAO XM, et al. Cardiac fibrosis and arrhythmo-genesis[J].Compr Physiol, 2017, 7(3):1009-1049.
    [5]
    张勇涛,蒋凡.生理性和病理性心肌肥厚的信号传导机制[J].中华心血管病杂志,2015,43(3):277-280.
    [6]
    MA Y, ZOU H, ZHU XX, et al. Transforming growth factor β: A potential biomarker and therapeutic target of ventricular remodeling[J]. Oncotarget, 2017,8(32): 53780-53790.
    [7]
    KONG P, CHRISTIA P, FRANGOGIANNIS NG.The pathogenesis of cardiac fibrosis[J].Cell Mol Life Sci, 2014,71(4):549-574.
    [8]
    宋冰,丁利.硫化氢抑制p38MAPK和NF-κB p65信号通路活性改善糖尿病心肌纤维化的作用和机制[J]. 解放军医学杂志,2016,41(11):902-907.
    [9]
    ARABACILAR P, MARBER M. The case for inhibiting p38 mitogen-activated protein kinase in heart failure[J].Front Pharmacol, 2015, 6:102.
    [10]
    DAVENPORT AP, HYNDMAN KA, DHAUN N, et al. Endothelin[J]. Pharmacol Rev, 2016, 68(2): 357-418.
    [11]
    JEN HL, LIU PL, CHEN YH, et al. Peroxisome proliferator-activated receptorα reduces endothelin-1-caused cardiomyocyte hypertrophy by inhibiting nuclear factor-κB and adiponectin[J]. Mediators Inflamm, 2016, 2016: 5609121.
    [12]
    WENG X, YU L, LIANG P, et al. A crosstalk between chromatin remodeling and histone H3K4 methyltransferase complexes in endothelial cells regulates angiotensin Ⅱ-induced cardiac hypertrophy[J]. J Mol Cell Cardiol, 2015,82: 48-58.
    [13]
    GONG X, MING X, DENG P, et al. Mechanisms regulating the nuclear translocation of p38 MAP kinase[J]. J Cell Biochem, 2010,110(6):1420-1429.
    [14]
    CHEN X, GAO B, PONNUSAMY M, et al. MEF2 signaling and human diseases[J]. Oncotarget, 2017, 8(67):112152-112165.
    [15]
    ZHAO M, NEW L, KRAVCHENKO VV, et al. Regulation of the MEF2 family of transcription factors by p38[J]. Mol Cell Biol,1999,19(1):21-30.
    [16]
    HAN J, JIANG Y, LI Z, et al. Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation[J]. Nature,1997,386(6622):296-299.
    [17]
    DADSON K, TURDI S, HASHEMI S, et al. Adiponectin is required for cardiac MEF2 activation during pressure overload induced hypertrophy[J]. J Mol Cell Cardiol, 2015, 86:102-109.
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (755) PDF downloads(544) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return