Lycium barbarum polysaccharide exhibits cardioprotection in an experimental model of ischemia-reperfusion damage

Abstract

Cardiovascular diseases are a major cause of mortality and disability worldwide. The present study investigated the cardio-protective effects of polysaccharides extracted from Lycium barbarum (LB), the fruit of which is traditionally used in Chinese medicine. Polysaccharides were characterized using Fourier transform infrared spectroscopy and high‑performance liquid chromatography techniques. The present study demonstrated that LB polysaccharides are composed of glucose and fructose monosaccharides in a molar ratio of 1:2. A total of 36 rats were divided into three groups plus a control group, with nine animals in each group, and were used for studying the cardioprotective effects of LB polysaccharides. The low‑dose group received 150 mg/kg body weight (BW) polysaccharides and the high‑dose group received 300 mg/kg BW polysaccharides. The results demonstrated that the LB polysaccharides reduced the levels of myocardial lactate dehydrogenase and increased the sodium‑potassium ATPase and calcium ATPase activities in rats with heart ischemia‑reperfusion injury. In addition, there was a decrease in the myocardial Bax‑positive expression and the rate of myocardial cell apoptosis, along with a dose‑dependent increase in Bcl‑2‑positive expression. Therefore, it was concluded that LB polysaccharides are able to halt the progression of cardiovascular diseases.

Lycium barbarum polysaccharides restore adverse structural remodelling and cardiac contractile dysfunction induced by overexpression of microRNA‐1

“…Till recent several years LBPs are given increasing attention in the field and most researches focus on its anti‐oxidative property as a free radical scavenger for immunomodulation and anticancer 14, 15, 16. The studies of LBPs on cardiovascular aspect are only limited to the protective phenomena (no discussion of mechanism) on doxorubicin‐induced cardiotoxicity and ischaemia/reperfusion injury of rat heart 21, 22, 23, 24. In the present study, we used the model of miR‐1 Tg mice and demonstrated that LBPs restored the cardiac function impaired by overexpression of miR‐1, as indicated by increase in EF, CO, ESP, and dp/dt max , as well as decrease in ESV and EDV.…”

“…[14][15][16] The studies of LBPs on cardiovascular aspect are only limited to the protective phenomena (no discussion of mechanism) on doxorubicin-induced cardiotoxicity and ischaemia/reperfusion injury of rat heart. [21][22][23][24] In the present study, we used the model of HF with complicated pathogenesis is associated with loss of cardiac contractility, abnormalities in Ca 2+ handling and altered phosphorylation states of cardiac contractile regulatory protein. 43,44 Our previous study has elucidated that overexpression of miR-1 repressed potential target proteins CaM and cMLCK, which attenuated the phosphorylation of CaMKII, cMyBP-C and MLC2v, leading to impaired sarcomeric assembly and consequent heart dysfunction.…”

“…Electrocardiographic and biochemical evidence were found that LBPs elicit a typical cardioprotective effect against Doxorubicin‐related oxidative stress in rats and dogs 21, 22. LBPs reduced myocardial apoptosis and injury in ischemia/reperfusion process of rat heart and could prevent the development of cardiovascular diseases 23, 24. However, until now, no available information has addressed the effects of LBPs on cardiac structure and function in HF.…”

“…21,22 LBPs reduced myocardial apoptosis and injury in ischemia/reperfusion process of rat heart and could prevent the development of cardiovascular diseases. 23,24 However, until now, no available information has addressed the effects of LBPs on cardiac structure and function in HF. Given its biological property, it is conceivable that LBPs may produce beneficial actions in preventing the development of HF and act as a potential therapy option.…”

Mechanism in bradycardia induced by Trimethyltin chloride: Inhibition activity and expression of Na⁺/K⁺-ATPase and apoptosis in myocardia

“…There- fore, it is believed that DLST protein is related to the production of ATP in heart tissue, which further affects the energy metabolism of the heart, leading to bradycardia (Keßler et al, 2015). A study showed that Lycium barbarum polysaccharide has a protective effect on the myocardial injury caused by ischemia-reperfusion, and the mechanism is that Lycium barbarum polysaccharide enhances the activity of the Na + /K + -ATPase and inhibits the apoptosis of myocardial cells (Hou et al, 2017). Ascleposide, as a type of cardiac glycoside, inhibits cell proliferation and promotes apoptosis.…”