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| Panax Notoginseng Saponins Inhibits Ventricular Remodeling after Myocardial Infarction in Rats Through Regulating ATF3/MAP2K3/p38 MAPK and NFκ B Pathway |
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| KeyWord:Panax notoginseng saponins, myocardial infarction, ventricular remodeling inflammation |
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| Abstract: |
| Objective: To explore whether Panax notoginseng saponins (PNS) exhibits heart protective effect in myocardial infarction (MI) rats and to identify the potential signaling pathways involved. Methods: MI rats induced by ligating the left anterior descending (LAD) coronary artery were assigned to sham coronary artery ligation or coronary artery ligation. Totally 36 Sprague-Dawley rats were randomly divided into sham group (distilled water, n=9), MI group (distilled water, n=9), PNS group (PNS, 40 mg/kg daily, n=9) and fosinopril group (FIP, 1.2 mg/kg daily, n=9) according to a random number table. The left ventricular morphology and function were conducted by echocardiography. Histological alterations were evaluated by the stainings of HE and Masson. The serum levels of C reactive protein (CRP), tumor necrosis factor α (TNF-α ), growth differentiation factor-15 (GDF-15) and the ratio of metalloproteinase-9 (MMP-9) and tissue inhibitor of MMP-9 (TIMP-1) were determined by ELISA. The levels of activating transcription factor 3 (ATF3), mitogen-activated protein kinase kinase 3 (MAP2K3), p38 mitogen-activated protein kinase (p38 MAPK), phosphorylation of p38 MAPK (p-p38 MAPK), transforming growth factor-β (TGF-β 1), collagen Ⅰ , nuclear factor kappa B p65 (NFκB p65), phosphorylation of NFκ B p65 (p-NFκ B p65), and phosphorylation of inhibitory kappa Bα (p-Iκ Bα ) in hearts were measured by Western blot and immunohistochemical staining, respectively. Results: PNS improved cardiac function and fibrosis in MI rats (P<0.05). The serum levels of CRP, TNF-α , GDF-15 and the ratio of MMP9/TIMP1 were reversed by PNS in MI rats. The expressions of TGF-β 1, collagen Ⅰ , MAP2K3, p38 MAPK, p-p38 MAPK, NFκ B p65, p-NFκ B p65, and p-Iκ Bα were down-regulated, while ATF3 increased with the treatment of PNS (P<0.05). Conclusions: PNS may improve cardiac function and fibrosis in MI rats via regulating ATF3/MAP2K3/p38 MAPK and NFκ B signaling pathways. These results suggest the potential of PNS in preventing the development of ventricular remodeling in MI rats. |
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