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[Beneficial effects of Schisandrin B on the cardiac structure and function in a mice model of myocardial infarction].

Objective: To investigate whether Schisandrin B (Sch B) could improve cardiac structure and function in myocardial infarction (MI) mice and related mechanisms. Methods: Male C57BL/6J mice were randomized into sham ( n =8), MI+ Sch B ( n =24, 80 mg·kg(-1)·d(-1) per gavage) or MI+ vehicle ( n =24, equal volume). After treatment for 3 weeks, cardiac function was detected by echocardiography measurement.Infarction size was measured by Evans blue and TTC staining.HE and Masson trichrome staining were used to observe the myocardial inflammation, structure and fibrosis.TNF-α, TGF-β, IL-1β were detected by ELISA. The apoptosis index of ischemic myocardial cells was detected by immunofluorescence. NF-κB, Bcl-2, Bax, Akt phosphorylated Akt(p-Akt), eNOS, phosphorylated eNOS (p-eNOS) were detected by Western blot. Results: Three weeks after operation, survival rate (83.33% vs. 54.17%, P <0.05), LVEF((51.77±8.50)% vs.(40.23±8.30)%, P <0.05), LVFS((26.44±5.15)% vs. (19.53±4.56)%, P <0.05)were significantly higher; LVEDD ((4.13±0.40) mm vs.(4.44±0.46)mm, P <0.05), LVESD((3.07±0.39) mm vs. (3.46±0.52)mm, P <0.05), the heart weight/body weight ratio((0.59±0.06)% vs. (0.68±0.10)%, P <0.05)was significantly lower and infarct size ((23.4±2.36)% vs. (39.4±2.06)%, P <0.05) was significantly reduced in MI+ Sch B group than those in MI+ vehicle group. In MI+ vehicle group, HE staining showed a large number of inflammatory cells in the peri-infarctl region, and the permutation structure was very disorganized, while above changes were significantly reduced in the MI+ Sch B group. Masson staining results showed that the degree of myocardial fibrosis in MI+ Sch B group was significantly less than that of MI+ vehicle group.Moreover, Sch B could down-regulate some inflammatory cytokines, like NF-κB、TGF-β、TNF-α and IL-1β, activate Akt-eNOS pathway, upgrade Bcl-2 and downgrade Bax and reduce cell apoptosis as compared with MI+ vehicle group (all P <0.05). Conclusions: Our results demonstrate that Sch B can reduce inflammation, inhibit apoptosis, and attenuate cardiac remodeling and improve cardiac function in this mice MI model.Sch B might serve as a potential novel therapeutic agent for ischemic heart disease.

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