Suxiao Jiuxin Pills Prevent Ventricular Fibrillation from Inhibiting L-type Calcium Currents CaV1.2 in vivo and in vitro.
10.1007/s11655-022-3623-7
- Author:
Jian-Yong QI
1
;
Dong-Yuan KANG
1
;
Juan YU
2
;
Min-Zhou ZHANG
3
,
4
Author Information
1. Acute Myocardial Infarction Key Laboratory of Chinese Medicine in Guangzhou, the 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Province Hospital of Chinese Medicine, Guangzhou, 510006, China.
2. Animal Center, the 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Province Hospital of Chinese Medicine, Guangdong Province Academy of Chinese Medicine, Guangzhou, 510006, China.
3. Acute Myocardial Infarction Key Laboratory of Chinese Medicine in Guangzhou, the 2nd Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Province Hospital of Chinese Medicine, Guangzhou, 510006, China. mingzhouzhang8@
4. com.
- Publication Type:Journal Article
- Keywords:
CaV1.2;
Suxiao Jiuxin Pills;
patch clamp;
simulation;
ventricular fibrillation
- MeSH:
Animals;
Rabbits;
Mice;
Calcium;
Computer Simulation;
Arrhythmias, Cardiac;
Electrocardiography
- From:
Chinese journal of integrative medicine
2023;29(2):108-118
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To investigate whether Suxiao Jiuxin Pills (SJP), a Chinese herbal remedy, is an anti-ventricular fibrillation (VF) agent.
METHODS:VF was induced by isoproterenolol (ISO) intraperitoneal injection followed by electrical pacing in mice and rabbits. The effects of SJP on the L-type calcium channel current (CaV1.2), voltage-dependent sodium channel current (INa), rapid and slow delayed rectifier potassium channel current (IKr and IKs, respectively) were studied by whole-cell patch-clamp method. Computer simulation was implemented to incorporate the experimental data of SJP effects on the CaV1.2 current into the action potential (AP) and pseudo-electrocardiography (pseudo-ECG) models.
RESULTS:SJP prevented VF induction and reduced VF durations significantly in mice and rabbits. Patch-clamp experiments revealed that SJP decreased the peak amplitude of the CaV1.2 current with a half maximal concentration (IC50) value of 16.9 mg/L (SJP-30 mg/L, -32.8 ± 6.1 pA; Verapamil, -16.2 ±1.8 pA; vs. control, -234.5 ±16.7 pA, P<0.01, respectively). The steady-state activation curve, inactivation curve, and the recovery from inactivation of the CaV1.2 current were not shifted significantly. Specifically, SJP did not altered INa, IKr, and IKs currents significantly (SJP vs. control, P>0.05). Computer simulation showed that SJP-reduced CaV1.2 current shortened the AP duration, transiting VF into sinus rhythm in pseudo-ECG.
CONCLUSION:SJP reduced VF via inhibiting the CaV1.2 current with in vivo, in vitro, and in silico studies, which provide experimental basis for SJP anti-VF clinical application.
