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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-β1),collagen Ⅰ,nuclear factor kappa B p65 (NFκB p65),phosphorylation of NFκB p65 (p-NFκB 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-β1,collagen Ⅰ,MAP2K3,p38 MAPK,p-p38 MAPK,NFκB p65,p-NFκB p65,and p-IκBα 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 NFκB signaling pathways.These results suggest the potential of PNS in preventing the development of ventricular remodeling in MI rats.