مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

video

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

sound

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Persian Version

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

View:

14
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Download:

9
مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Cites:

Information Journal Paper

Title

Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κ, B signaling pathway

Pages

  114-120

Abstract

 Objective(s): To investigate the effect of mogroside IIIE (MGIIIE) on isoproterenol (ISO)-induced Myocardial fibrosis and explore its possible mechanisms. Materials and Methods: Forty C57BL/6 male mice (6-8 weeks) were randomly divided into a control group (n=10), model group (n=10), low MGIIIE dose group (n=10), and high MGIIIE dose group (n=10). Myocardial fibrosis was established By subcutaneous ISO injection. After 2 weeks of continuous gastric administration of MGIIIE, the cardiac structure was evaluated By echocardiography. Myocardial Inflammation and fibrosis were evaluated By histology examination. Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), p-Iκ, Bα, , p-NF-κ, B, transforming growth factor β, 1 (TGF-β, 1), and α,-smooth muscle actin (α,-SMA) expression were detected By western Blot. Inflammatory Cytokines (IL-1β, , IL-6, and TNF-α, ) in the serum were examined By ELISA. In the in vitro study, Ang II (1 μ, mol/l) was used to stimulate the fibroblasts, then Inflammation and fibrosis index were detected. Results: MGIIIE inhibited Inflammation and fibrosis and down-regulated TLR4, MyD88, TGF-β, 1, and α,-SMA expression in the myocardium. In the in vitro study, MGIIIE ameliorates the deposition of Col Ш,and Col I and decreases the release of inflammatory Cytokines. MGIIIE increased p-Iκ, Bα,and reduced p-NF-κ, B expression Both in vivo and in vitro. Conclusion: MGIIIE plays a role in anti-Myocardial fibrosis, By inhibiting TLR4/MyD88/NF-κ, B signaling expression, and decreasing inflammatory Cytokine release. MGIIIE may represent a novel therapeutic strategy for treating cardiac fibrosis.

Cites

  • No record.

    • References

    Cite

    APA: Copy

    Yanan, Shi, Bohan, Li, Shuaifeng, Sun, Wendan, Tian, & WEI, LIU. (2023). Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κ, B signaling pathway. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, 26(1), 114-120. SID. https://sid.ir/paper/1084950/en

    Vancouver: Copy

    Yanan Shi, Bohan Li, Shuaifeng Sun, Wendan Tian, WEI LIU. Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κ, B signaling pathway. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2023;26(1):114-120. Available from: https://sid.ir/paper/1084950/en

    IEEE: Copy

    Shi Yanan, Li Bohan, Sun Shuaifeng, Tian Wendan, and LIU WEI, “Inhibition of Mogroside IIIE on isoproterenol-induced myocardial fibrosis through the TLR4/MyD88/NF-κ, B signaling pathway,” IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, vol. 26, no. 1, pp. 114–120, 2023, [Online]. Available: https://sid.ir/paper/1084950/en

    Related Journal Papers

  • No record.

    • Related Seminar Papers

  • No record.

    • Related Plans

  • No record.

    • Recommended Workshops






    Move to top
    telegram sharing button
    whatsapp sharing button
    linkedin sharing button
    twitter sharing button
    email sharing button
    email sharing button
    email sharing button
    sharethis sharing button