Synergistic and Attenuating Effect of Electroacupuncture on Aconitine in Improving Heart Failure and Its Calcium Regulation Mechanism

Chen Zhou; Mozheng Wu; Qun Liu; Juan-Juan Xin; Shuang Wu; Yu-Xue Zhao; Wenxi Zhang; Xiao-Chun Yu; Jun-Hong Gao

doi:10.1155/2022/4940745

July 14, 2022Evidence-based Complementary and Alternative MedicineOpen Access

Synergistic and Attenuating Effect of Electroacupuncture on Aconitine in Improving Heart Failure and Its Calcium Regulation Mechanism

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Why the study?

The study was designed to observe the synergistic and attenuating effects of electroacupuncture on aconitine in improving heart failure and to explore its underlying calcium regulation mechanism.

Does electroacupuncture combined with aconitine improve heart failure and regulate calcium mechanisms in a rat model?

Structured PICO

Does electroacupuncture combined with aconitine improve heart failure and regulate calcium mechanisms in a rat model?

P

Population

24 male Sprague-Dawley rats with heart failure model

I

Intervention

Aconitine (ACO) combined with electroacupuncture (EA)

C

Comparator

Normal control (NC), untreated heart failure (HF) model, and Aconitine (ACO) alone

O

Outcome

Hemodynamic and echocardiographic parameters (LVSP, ±dp/dtmax, LVEF, LVFS), arrhythmia incidence and degree, and protein expressions of SERCA2a, PLB, and NCX1surrogate

Electroacupuncture synergizes with aconitine to improve cardiac function in a rat model of heart failure, potentially by enhancing SERCA2a activity and decreasing PLB and NCX1 expression.

Implication

EA + ACO may improve rat HF parameters; hypothesis-generating for calcium mechanisms, human trials needed.

Abstract

Objective. The objective is to observe the synergistic and attenuating effect of electroacupuncture (EA) on aconitine (ACO) in improving heart failure (HF) and to explore its underlying mechanism for calcium regulation. Methods. Twenty-four male Sprague-Dawley rats were randomly divided into four groups: normal control (NC) (n = 6), HF(n = 6), ACO (n = 6), and ACO + EA (n = 6). The maximum rates of left ventricular pressure rising and declining (±dp/dtmax), arrhythmia, the left ventricular systolic pressure (LVSP), ejection fraction (LVEF), and fractional shortening (LVFS) were measured by physiological recorder and ultrasound, respectively. Protein expressions of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA2a), phospholamban (PLB), and Na+-Ca2+ exchange (NCX1) in the left ventricle tissue were detected by fluorescence immunoblotting. Results. Compared with the NC group, LVSP, ±dp/dtmax, LVEF, and LVFS were decreased in the HF group; compared with the HF group, LVSP, ±dp/dtmax, LVEF, and LVFS were significantly increased in the ACO + EA group. Compared with the ACO group, the incidence and the degree of arrhythmia were significantly reduced in the ACO + EA group. Compared with the NC group, the activity of SERCA2a was decreased, and the expression of PLB and NCX1 was enhanced in the HF group; compared with the HF group and ACO group, the activity of SERCA2a was increased, and the expression of PLB and NCX1 was significantly attenuated in the ACO + EA group. Conclusions. EA plays a synergistic and attenuated role in ACO improving HF, and the mechanism may be related to the enhancement of the SERCA2a activity and the decrease of the expression of PLB and NCX1 in cardiomyocytes.