Toxicity-efficacy converting of ginseng combined with Fuzi Banxia incompatibility in heart failure stage of cor pulmonale

Objective: Fuzi Banxia is one of eighteen antagonisms, previous studies have shown that the incompat- ibility could play special effects in the specific condition of diseases and appropriate compatible envi- ronment. The present study aims to evaluate the toxicity-efficacy of ginseng combined with Fuzi Banxia incompatibility intervening in the heart failure stage of cor pulmonale and to explore its mechanism. Methods: Monocrotaline (MCT)-induced cor pulmonale were used in this study. Ultra high-resolution small animal ultrasound real-time imaging system and the right heart catheterization were used to es- timate cardiac function. Semi automatic biochemical analyzer was used to test myocardial enzyme LDH, CK, and CK-MB in serum. The heart tissues were stained with HE, and TUNEL assay was used to assess the pathomorphological changes and myocardial apoptosis. The expression of hypertrophy and apop- tosis associated genes: ANP, BNP, β-MHC, Bax, and Bcl-2 in the right ventricle were determined by RT-PCR. Results: Fuzi Banxia combined with ginseng obviously attenuated mortality, decreased RVHI, and in- creased cardiac index; RVSP and mPAP were significantly reduced, and EF and FS were raised obvi- ously; Myocardial enzymes LDH, CK, and CK-MB were pronounced attenuated; heart diameter reduced, right ventricular dilatation was significantly decreased, inflammatory cell infiltration notably reduced, and cardiac apoptosis rate was decreased obviously. Meanwhile, the expression of hypertrophy-related ANP, BNP, and β-MHC mRNA were up-regulated, the expression of apoptosis-related Bax mRNA was down-regulated, and the expression of anti-apoptosis-related Bcl-2 mRNA and Bcl-2/Bax ratio were up- regulated. Conclusion: Ginseng compatible environment could attenuate cardiac toxicity of Fuzi Banxia incompati- bility intervening in the heart failure stage of cor pulmonale, and improve cardiac function, which may be related to the expression of hypertrophy and apoptosis associated genes, and thus delay the occurrence and development of heart failure.