[Retracted] Insight into the Protective Effect of Salidroside against H2O2‐Induced Injury in H9C2 Cells

Abstract

Salidroside is the important active ingredient of Rhodiola species, which shows a wide range of pharmacological activities such as antioxidative stress, anti-inflammation, and antiliver fibrosis. In this paper, we aimed to study the protective effect and mechanism of salidroside against H2O2-induced oxidative damage in H9C2 cells by determining cell proliferation rate, intracellular reactive oxygen species (ROS) level, antioxidant enzyme activities, and the expression of apoptosis-related proteins. The results showed that salidroside significantly alleviated cell growth inhibition induced by H2O2 treatment in H9C2 cells, decreased the levels of intracellular ROS and malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD) and catalase (CAT); meanwhile, salidroside upregulated the expression of Bcl-2 while downregulated the expression of Bax, p53, and caspase-3 in H2O2-treated H9C2 cells. Furthermore, the antiapoptotic effect of salidroside was almost eliminated by the knockdown of Bcl-2. In the further exploration, the Bcl-2 expression was decreased by the p53 overexpression and increased by p53 knockdown in H2O2-treated H9C2 cells. Consequently, salidroside could protect H9C2 cells against H2O2-induced oxidative damage, and the underlying mechanism may be related to scavenging intracellular ROS, increasing the activities of intracellular antioxidant enzymes and inhibiting the expression of apoptosis-related proteins.

Salidroside Ameliorates Ultraviolet-Induced Keratinocyte Injury by Inducing SIRT1-Dependent Autophagy

“… 26 SAL shows antioxidant effect on cardiomyocytes, which can significantly reduce the inhibitory effect of H 2 O 2 on the growth of H9c2 cells, and reduce the cellular levels of ROS and MDA, and improve the activities of SOD and catalase (CAT). 27 Atherosclerosis is a chronic vascular inflammatory disease associated with oxidative stress. In an in vitro model of human umbilical vein endothelial cells (HUVEC) induced by oxidized low-density lipoprotein (ox-LDL), SAL treatment protected HUVEC from damage by inhibiting oxidative stress and improving mitochondrial dysfunction, 28 and protected against ox-LDL-induced endothelial injury and oxidative stress by enhancing autophagy mediated by SIRT1-FoxO1 pathway.…”

Retracted: Insight into the Protective Effect of Salidroside against H2O2-Induced Injury in H9C2 Cells

“…This article has been retracted by Hindawi, as publisher, following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of systematic manipulation of the publication and peer-review process.…”