Fuzi and Banxia Combination, Eighteen Antagonisms in Chinese Medicine, Aggravates Adriamycin‐Induced Cardiomyopathy Associated with PKA/β2AR‐Gs Signaling

Fengjiao Sun; Yingying Huang; Lili Li; Chao Yang; Pengwei Zhuang; Yanjun Zhang

doi:10.1155/2018/2875873

January 1, 2018Evidence-based Complementary and Alternative MedicineOpen Access

Fuzi and Banxia Combination, Eighteen Antagonisms in Chinese Medicine, Aggravates Adriamycin‐Induced Cardiomyopathy Associated with PKA/β2AR‐Gs Signaling

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Why the study?

Does the combination of Fuzi and Banxia aggravate adriamycin-induced cardiomyopathy in a rat model?

Structured PICO

Does the combination of Fuzi and Banxia aggravate adriamycin-induced cardiomyopathy in a rat model?

P

Population

Adriamycin (ADR)-induced rat model of cardiomyopathy

I

Intervention

Combination of Aconite Lateralis Radix Praeparata (Fuzi) and Pinelliae Rhizoma (Banxia)

C

Comparator

Fuzi alone and Banxia alone

O

Outcome

Heart dysfunction, QT/QTc prolongation, cardiac apoptosis, and PKA/β2AR-Gs signaling protein expressionsurrogate

The combination of Fuzi and Banxia aggravates adriamycin-induced cardiomyopathy in rats by promoting cardiac apoptosis and QT prolongation, supporting traditional Chinese medicine contraindications.

Implication

May support Fuzi-Banxia in ADR cardiomyopathy models; leaves open clinical translation.

Abstract

Aconite Lateralis Radix Praeparata (Fuzi) and Pinelliae Rhizoma (Banxia) are a combination often used to treat cardiovascular diseases in ancient and modern clinical practice. However, eighteen antagonisms based on traditional Chinese medicine (TCM) theory often abided against such combination therapy. Therefore, exploring whether coadministration of the two herbs can be used in adriamycin‐ (ADR‐) induced cardiomyopathy and clarifying the potential mechanism could help to guide its clinical application. Echocardiography experiments revealed that either Fuzi, Banxia, or their combination had effect on ADR‐induced heart dysfunction, while high dose Fuzi exerted positive inotropic effect associated with restored PKA levels. Moreover, low dose Fuzi significantly reduced QT/QTc prolongation, inhibited cardiac apoptosis, and upregulated protein expression of PKA. However, combination of Fuzi and Banxia greatly aggravated QT/QTc prolongation and cardiomyocyte apoptosis in ADR rats compared with each drug alone, which was accompanied by a marked decrease in PKA, pSer346 levels. Similarly, Banxia alone treatment promoted cardiac apoptosis and downregulated protein levels of PKA and pSer346. Additionally, high dose Fuzi treatment also produced proapoptotic effect. Taken together, our study has provided the first direct evidence that combination of Fuzi, a positive inotropic agent, with Banxia promoted cardiac apoptosis in an ADR induced rat model of cardiomyopathy, which may be associated with suppression of PKA/ β 2AR‐Gs signaling. This study also provides scientific language for better understanding of the risks and limitations of combination of Fuzi and Banxia in clinical applications.