Effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning on ventricular arrhythmias induced by acute ischemia‑reperfusion in rats

DU Qin; CHAI Hong; LI Xiaohong; HUANG Xueyuan; ZHOU Chengzhi; ZHAN Na

doi:10.14188/j.1671-8852.2024.0430

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Effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning on ventricular arrhythmias induced by acute ischemia‑reperfusion in rats

更新时间：2026-11-05

- Effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning on ventricular arrhythmias induced by acute ischemia‑reperfusion in rats
- Medical Journal of Wuhan University Vol. 46, Issue 4, Pages: 438-445(2025)
- 作者机构：
  
  1.武汉大学人民医院护理部湖北武汉 430060
  2.华中科技大学同济医学院病理生理学系湖北武汉 430030
  3.石首市人民医院病理科湖北石首 434400
- 作者简介：
- 基金信息：
- DOI：10.14188/j.1671-8852.2024.0430
  CLC： R541.7
- Received：04 June 2024，
  
  Published：25 April 2025
- 稿件说明：
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杜勤,柴红,李小红等.人参皂苷Rb1缺血后处理对急性缺血再灌注室性心律失常的影响及其机制探讨[J].武汉大学学报（医学版）,2025,46(04):438-445.

DU Qin,CHAI Hong,LI Xiaohong,et al.Effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning on ventricular arrhythmias induced by acute ischemia‑reperfusion in rats[J].Medical Journal of Wuhan University,2025,46(04):438-445.
杜勤,柴红,李小红等.人参皂苷Rb1缺血后处理对急性缺血再灌注室性心律失常的影响及其机制探讨[J].武汉大学学报（医学版）,2025,46(04):438-445. DOI： 10.14188/j.1671-8852.2024.0430.

DU Qin,CHAI Hong,LI Xiaohong,et al.Effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning on ventricular arrhythmias induced by acute ischemia‑reperfusion in rats[J].Medical Journal of Wuhan University,2025,46(04):438-445. DOI： 10.14188/j.1671-8852.2024.0430.

摘要

目的

探讨人参皂苷Rb1缺血后处理（Rb1‑IPost）对急性缺血再灌注（I/R）室性心律失常的影响及其机制。

方法

将SPF级SD雄性大鼠分为对照组（Control组，

=15）、急性缺血再灌注（I/R组，

=15）和Rb1‑IPost组（Rb1‑IPost组，

=15）。利用Langendorff心脏灌流系统建立大鼠离体心脏急性I/R模型，通过记录左室发展压（LVDP）和冠状动脉压，测定心脏左室发展压的恢复和再灌注痉挛度，观察心跳状态特征，评价心功能变化；记录左心室游离壁单相动作电位（MAP），观察MAP主要参数的幅度（APA）、最大上升速率（Max

dv/dt

）、复极化恢复到10%、20%、50%、90%时间（APD

、APD

），以及复极化时程三角测量值（Triangulation）差异；应用短阵快速刺激，记录诱发室性心律失常的刺激周长（BCL）、发生率和持续时间；酶解法分离单个心室肌细胞，全细胞膜片钳技术记录心室肌细胞膜上L‑型钙电流（I

Ca‑L

）大小和动力学特征改变。

结果

与I/R组比较，Rb1‑IPost组LVDP的恢复显著回升[(22.82±4.97)%

(90.04±11.61)%

]

，再灌注痉挛度明显降低[(93.81±8.05)

（20.08±8.47）mmHg

]

（均

0.01）。I/R后心脏跳动波形变得高翘、耸起，心跳参差不齐，心律失常显著增多，但经Rb1‑IPost处理后，缺血后心脏跳动逐步恢复至规则、平稳，心律失常诱发减少直至恢复正常；而且，Rb1‑IPost组大鼠心脏出现明显的APA增加，Max

dv/dt

增快，以及APD

、APD

和Triangulation均显著缩短（均

0.01）；另外，缺血心脏经过Rb1‑IPost作用，被诱发室性心律失常的BCL和持续时间明显缩短、诱发率显著下降（均

0.01），Rb1‑IPost组心脏能经受显著缩短的刺激周长，且仅能被诱发传导时间明显缩短的短阵局部触发电活动并很快转为正常。最后，在钳制电压下，Rb1‑IPost组心室肌细胞I

Ca‑L

在各钳制电压下均明显减少，当钳制电压为+20 mV时，其I

Ca‑L

电流密度由（11.06±0.51）pA/pF减小为（6.09±0.23）pA/pF（

0.01），降低幅度超过57%。且Rb1‑IPost组心室肌细胞I

Ca‑L

的I‑V曲线显著抬高，明显高出I/R组I

Ca‑L

的I‑V曲线。

结论

Rb1‑IPost能显著改善I/R心脏的心功能，纠正电重构，具有抗I/R损伤及其室性心律失常作

用，其电生理机制可能与Rb1‑IPost明显减少心室肌细胞I

Ca‑L

大小，防治Ca

超载，从而降低I/R室性心律失常的易感性密切相关。

Abstract

Objective

To investigate the effects and mechanism of Ginsenoside Rb1‑ischaemia postconditioning (Rb1‑IPost) on ventricular arrhythmias induced by acute ischemia‑reperfusion (I/R) in rat hearts

in vitro

Methods

The SPF male Sprague‑Dawley rats were randomly divided into the control group (Control group

=15)

acute ischemia‑reperfusion group (I/R group

=15)

and Ginsenoside Rb1‑ischaemia postconditioning group (Rb1‑IPost group

=15). The acute I/R heart models were setup by using the Langendorff‑perfusion heart system in rats

in vitro

. To record left ventricular developed pressure (LVDP) and coronary artery pressure as well as heart heat status

the myocardiac function was evaluated by measuring recovery of LVDP and contractural magnitude of reperfusion as well as observing the characteristics of heart heat status. The main electrical parameters in 3 groups were recorded such as APA

Max

dv/dt

APD

and Triangulation from recording of monophasic action potential (MAP)

as well as basic cycle lenth (BCL)

incidence and duration of ventrucular arrhythmias induced by burst‑pacing in left ventricualar tissue of rats

in vivo

. The L‑type calcium channel (I

Ca‑L

) and its current‑voltage curve (I‑V curve) were recorded via whole‑cell patch clamp technique in enzymatically dissociated single rats's ventricular myocytes.

Results

Compared with those in I/R group

the recovery of LVDP was significantly upgraded

as (22.82±4.97)%

(90.04±11.61)%

and the contractural magnitude of reperfusion was obviously reduced as (93.81±8.05)

(20.08±8.47

) mmHg

in rat hearts of Rb1‑IPost group (all

0.01

respectively). The heartbeat waveform becomes elevated and protruding after I/R

with irregular and uneven heartbeats and a significant increase in arrhythmias. However

after treatment with Rb1⁃IPost

the post⁃ischemic heartbeats gradually return to a regular and stable pattern

and the induction of arrhythmias is reduced until normalcy is restored. Furthermore

Rb1‑IPost could significantly increase APA and Max

dV/dt

as well as shorten APD

APD

and Triangulation in rat hearts of Rb1‑IPost group i

n vitro

(all

0.01

respectively). Otherwise

Rb1‑IPost could markedly shorten BCL and persistence time

as well as decrease the inducing rate of ventricular arrhythmias with burst‑pacing in Rb1‑IPost group in rat hearts

in vitro

(all

0.01

respectively). Finally

with the voltage clamp model

Rb1‑IPost in ventricular myocytes of Rb1‑IPost group could significantly decrease the value of I

Ca‑L

at different command potential in rats. At the +20 mV of command potential from -40 mV of voltage clamp

the current densities of I

Ca‑L

were significantly decreased from (11.06±0.51) pA/pF in I/R group to (6.09±0.23) pA/pF (

0.01)

and the amplitude of reducing could amount to 57% in Rb1‑IPost group in rats. Moreover

Rb1‑IPost could completely elevate the I‑V curve of I

Ca‑L

upwards other goups without altering the I‑V curve direction in ventricular myocytes of Rb1‑IPost group in rats.

Conclusion

Rb1‑IPost could significantly improve the cardiac performance and rectify the electrical remodeling so that to provide the effects of anti‑acute I/R ventricular arrhythmias of inducing by myocardial I/R injury in rat hearts. It was suggested that the mechanism of Rb1‑IPost inhibiting acute I/R ventricular arrhythmias might attribute to

that Rb1‑IPost could markedly decrease influx of I

Ca‑L

and provent to Ca

overload

which to contricute to diminishing the susceptibility of ventricular arrhythmia induced by acute I/R hurt.

关键词

Keywords

references

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