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        20(S)-ginsenoside Rg3 exerts anti-fi brotic effect after myocardial infarction by alleviation of fi broblasts proliferation and collagen deposition through TGFBR1 signaling pathways

        Honglin Xu,Haifeng Miao,Guanghong Chen,Guoyong Zhang,Yue Hua,Yuting Wu,Tong Xu,Changlei Hu,Mingjie Pang,Leyi Tan,Xin Han,Bin Liu,Yingchun Zhou 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6

        Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiacremodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovasculardiseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effectpost-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-b1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin andMasson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effectsof Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 wasexplored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice andTGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiacfunction. Rg3-TGFBR1 had the 1.78 10 7 M equilibrium dissociation constant based on SPRi analysis,and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulatedthe TGF-b1-mediated CFs growth together with collagen production in vitro through TGFBR1signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferationalong with collagen deposition by inactivation of TGFBR1 pathway.

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