Objective To determinate the effects of sodium tanshinone ⅡA sulfonate(STS)on cardiomyocyte hypertrophy and explore the relative effects of STS on mitogen-activated protein kinase signal transduction system in rats with cardiomyocyte hypertrophy through constricting the thoracic aorta.Methods The models of cardiomyocyte hypertrophy were established in vivo,and the thoracic aorta was partially tied between the right innominate and the left common carotid arteries.The rats were randomly divided into 6 groups(n=8/group)as follows:①sham,②transverse aortic constriction(TAC),③TAC+low-dose Tan(TAC+LT)(5 mg/kg),④TAC+middle-dose Tan(TAC+MT)(10 mg/kg),⑤TAC+high-dose Tan(TAC+HT)(20 mg/kg),and ⑥ TAC+Val(10 mg/kg).After treatment for 8 weeks,echocardiography was performed to observe the changes in hypertrophy and heart function,and heart samples were cut into transverse sections and stained with hematoxylin and eosin(H&E).The MAPKs protein expression in the cardiomyocytes was detected by Western blot.Results The heart weight index(HWI),left ventricular mass index(LVMI)and cross-sectional diameter of cardiomyocytes(CD),left ventricular posterior wall thickness(LVWT),and interventricular septal thickness(IVS)were significantly increased in TAC group as compared with sham group.The relative parameters in STS groups and Val group were reduced as compared with those in TAC group.Western blot analysis revealed the p-ERK and p-p38 expression was significantly decreased in TAC group as compared with sham group(P＜0.01).The p-ERK expression was significantly decreased in STS groups and Val group as compared with TAC group(P＜0.05).The TAC+HT group,TAC+MT group and Val group had significantly higher p-p38 expression than TAC group(P＜0.05).Conclusion Tanshinone ⅡA could regulate the expression of protein in MAPK pathway to exert its inhibitory effects on hypertrophy of cardiomyocytes.

BACKGROUND:As one of the main active ingredients in epimedium, icari n plays an important role in bone defect repair. Sustained and effective concentration of icari n in vivo is essential for bone damage repair.
OBJECTIVE:To recommend the research progress of epimedium glycoside for bone repair and to explore the pharmaco-active concentration of icari n.
METHODS:A computer-based online search of CNKI database (http://www.cnki.net/) and PubMed database (http://www.ncbi.nlm.nih.gov/PubMed) from January 2000 to October 2013 was performed for related articles of the effect of icari n for bone defect repair and bone damage repair. The key words were“icari n, concentration, bone”in Chinese and English. After repeated articles were excluded, 76 related articles were screened out and 44 of them met the inclusive criteria.
RESULTS AND CONCLUSION:The icari n-released scaffold materials can induce the osteogenic differentiation of bone marrow-derived mesenchymal stem cells, promote the viability of osteoblasts and inhibit the resorption of osteoclasts, thus repairing bone tissue. It is certain that icari n promotes cellular dif erentiation, however whether it can promote cellular proliferation remains unclear. The pharmaco-active concentration of icari n ranges from10-8 to 10-5 mol/L, but clinical trial has not yet been carried out, and specific drug concentration is uncertain, which needs further exploration.