Abstract

Dangguibuxue decoction (DBD), a kind of Chinese herbal medicine, has been widely used to treat blood deficiency disease in China. In this experiment, we studied the effects of the Dangguibuxue decoction (DBD) on the myocardial injury induced by cyclophosphamide in mice. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and lactic dehydrogenase (LDH) in serum were detected by commercial kits. Total white blood cell (WBCs), platelets, and cytokines pathological changes of heart tissue were also examined. In addition, the protein levels of the NF-кB pathway were detected to reveal its mechanism. The results showed that DBD significantly decreased the levels of ALT, AST, CK, and LDH and increased WBCs in CTX-induced mice. In addition, DBD significantly alleviated pathological changes of heart tissue. DBD significantly reduced the protein expressions of NF-кB signaling pathway. In summary, DBD can be considered an effective drug to alleviate CTX-induced heart damage in mice.

Highlights

  • Cardiovascular disease, a severe health problem, is recognized as one of the most burdensome diseases of society

  • Compared with the control group, the spleen weights of the mice that were injected alone with CTX shown decreased, while the mice injected with CTX along with two doses of Dangguibuxue decoction (DBD) presented a marked elevation (p

  • High doses DBD (12 g/kg) treatment facilitated the spleen weight growth, suggesting DBD seemed to exhibit its effect in conjunction with spleen function (Figure 2)

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Summary

Introduction

Cardiovascular disease, a severe health problem, is recognized as one of the most burdensome diseases of society. Cyclophosphamide (CTX), an alkylating agent, is a widely acknowledged anticancer chemotherapeutic agent used alone or in combination with other medicines for part of the mainstream therapy of several human malignancies [2]. Due to its immunosuppressive activity, CTX could be used in preconditioning the host for immunotherapy. Emerging evidence elicited that the administration with CTX increased the numbers of the dendritic cells that directly drove the immune response and activation of immune-reaction by promoting the mobilization of the hematopoietic stem cells [3]. Several adverse side effects of CTX have been reported, such as heart toxicity with high incidence. Exposure to high dose CTX could attribute to the acute cardiotoxic effects characterized by myocyte damage, extravasation of toxic metabolites, and diastolic contractile dysfunction [4]. We employed the injection of CTX as an experimental model in our study

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