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  • Title: Cardioprotection of Sheng Mai Yin a classic formula on adriamycin induced myocardial injury in Wistar rats.
    Author: Zhang K, Zhang J, Wang X, Wang L, Pugliese M, Passantino A, Li J.
    Journal: Phytomedicine; 2018 Jan 01; 38():1-11. PubMed ID: 29425641.
    Abstract:
    BACKGROUND: Sheng Mai Yin (SMY), a well-known Chinese herbal medicine, is widely used to treat cardiac diseases characterized by the deficiency of Qi and Yin syndrome in China. SMY-based treatment has been derived from Traditional Chinese Medicine (TCM), officially recorded in the Chinese Pharmacopoeia. PURPOSE: We aimed to clarify whether SMY attenuates myocardial injury induced by adriamycin in Wistar rats with chronic heart failure (CHF). METHODS: To quantify ginsenoside Rg1, ophiopogonin D, ophiopogonin D', schisandrin by HPLC. To establish CHF animal model, adriamycin was intraperitoneally injected in Wistar rats for 7 weeks at a dose of 2 mg/kg body weight. Overall, 180 rats were randomly assigned to six groups: control, CHF model, captopril (positive control), high dose (HSMY), medium dose (MSMY), and low dose (LSMY). Experimental rats were fed 0.625 mg/kg captopril and 90 mg/kg, 45 mg/kg, and 22.5 mg/kg SMY, respectively, over 7 weeks. The inflammatory cytokines TNF-α and IL-6 were measured using ELISA. Matrix metalloproteinases (MMPs) were identified using immunohistochemistry (IHC). Both IHC and RT-PCR were used for quantification of COL-IV expression levels in the heart tissues. Scanning electron microscopy (SEM) was used for the visualization of myocardium morphology. RESULTS: The concentration of ginsenoside Rg1, ophiopogonin D, ophiopogonin D' and schisandrin in SMY was found to be 25.63 ± 3.42 mg, 11.00 ± 1.17 mg, 7.02 ± 0.51 mg, and 25.31 ± 4.28 mg per gram of SMY, respectively. Compared with CHF model group, TNF-α levels were significantly lower (p < .01) in the four drug-administered groups. Moreover, except in the SYM low dose group, IL-6 levels in the other 3 drug-administered groups were also significantly reduced (p < .01). COL-IV expression was also significantly reduced on treatment with high SYM dose (p < .05). IHC results confirmed that SMY and captopril significantly reduced MMPs expression in the heart. CONCLUSION: SMY could control or slow CHF progression by suppressing pathological changes in the myocardium in CHF models. This could be attributed at least partly to the downregulation of IL-6 and TNF-α and inhibition of overexpression of MMPs and COL-IV, which significantly relieved the cardiac-linked pathologies, decreased the risk of myocardial fibrosis, and inhibited cardiac remodeling. These findings suggested that SMY and captopril have similar efficacy for the treatment of adriamycin-induced myocardial injury. In addition, Chinese herbal preparation SMY may play a role in the treatment of cardiac diseases.
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