Combined Salvianolic Acid B and Ginsenoside Rg1 Exerts Cardioprotection against Ischemia/Reperfusion Injury in Rats

Abstract

Lack of pharmacological strategies in clinics restricts the patient prognosis with myocardial ischemia/reperfusion (I/R) injury. The aim of this study was to evaluate the cardioprotection of combined salvianolic acid B (SalB) and ginsenoside Rg1 (Rg1) against myocardial I/R injury and further investigate the underlying mechanism. I/R injury was induced by coronary artery ligation for Wistar male rats and hypoxia/reoxygenation injury was induced on H9c2 cells. Firstly, the best ratio between SalB and Rg1was set as 2:5 based on their effects on heart function detected by hemodynamic measurement. Then SalB-Rg1 (2:5) was found to maintain mitochondrial membrane potential and resist apoptosis and necrosis in H9c2 cell with hypoxia/reoxygenation injury. Companying with same dose of SalB or Rg1 only, SalB-Rg1 showed more significant effects on down-regulation of myocardial infarct size, maintenance of myocardium structure, improvement on cardiac function, decrease of cytokine secretion including TNF-α, IL-1β, RANTES and sVCAM-1. Finally, the SalB-Rg1 improved the viability of cardiac myocytes other than cardiac fibroblasts in rats with I/R injury using flow cytometry. Our results revealed that SalB-Rg1 was a promising strategy to prevent myocardial I/R injury.

Oxidative Stress and Salvia miltiorrhiza in Aging‐Associated Cardiovascular Diseases

“…Recent research shows that Sal A has antiapoptotic effects via activating ERK1/2 and downregulating c-Jun N-terminal kinase (JNK), with increased Bcl-2 and reduced Bax protein expression [112, 113]. A combination of SalB and ginsenoside Rg1 increases the viability of cardiac myocytes and reduces infarct size, thereby improving the functional parameters of the heart against I/R injury in rats [114]. The injection of SM containing water-soluble components such as Sal A shows a cardioprotective effect after infarction by inhibiting L-type Ca 2+ channels and decreasing the contractility of adult rat cardiac myocytes [115].…”

Effect of Salvianolic Acid B on Cardiac Muscle Damage Following Exhaustive Exercise in Rats

“…을 살펴보면 실험동물의 관상동맥 결찰에 의한 심근경색에 대해 심근세포의 자연사를 억제하고 11) , matrix metalloproteinase-9 (MMP-9) 작용을 억제하며 12) , malondialdehyde 활성을 억제하고 13) , 사이토카인 분비를 억제하는 작용에 의 해 심근경색의 크기를 줄이며 심장의 기능과 구조적 손상을 보호한다고 하였다 14,15) . 그러나 심근경색 이외의 다양한 심 장손상에 대한 SAB의 작용에 대해서는 더 많은 연구가 필 요하다.…”

Myocardial Ischemia-Reperfusion Injury: The Perioperative Application and Cardiac Protective Potential of Ginsenoside Preparations

“…Ginseng total saponin, consisting of various ginsenosides, has been shown to attenuate MI/R injury by increasing the levels of anti-inflammatory molecules such as interleukin-10 (IL-10), and suppressing pro-inflammatory molecules such as IL-1β and IL-6 (31). Furthermore, another study (39) conducted in experimental I/R injury models both in vivo and in vitro evaluated the cardioprotective effects of combinational use of ginsenoside Rg1 and salvianolic acid B (SalB), the main active ingredients of Salviae miltiorrhizae on post-ischemic myocardial injury. Compared with a single dose of SalB or Rg1 alone, SalB-Rg1 combination was more potent to limit myocardial infarct size and down-regulate cytokine secretion including tumor necrosis factor-α (TNF-α) and IL-1β, and suppress the release of soluble vascular cell adhesion molecule-1 (sVCAM-1), a molecule that contributes to the increased vascular permeability induced by I/R injury (33,40,41).…”

“…Another study reported that pretreatment with ginsenoside Rd also exerted cardioprotective effects both in vivo and in vitro, as evidenced by limited infract size and decreased cellular apoptosis, concomitant with stabilized mitochondrial membrane potential and inhibited cytosolic translocation of mitochondrial Cyt-c via activating protein kinase B (Akt)/glycogen synthase kinase 3β (GSK3β) pathway (52). Other ginsenoside molecules, such as ginsenoside Rg1, Re, Rb1, have also been proved to attenuate MI/R injury by modulating apoptotic-associated pathways (28,39,(53)(54)(55).…”