Abstract
Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.
Highlights
Oxidative stress is defined as an excessive production of reactive oxygenated species that cannot be counteracted by the action of antioxidants, and as a perturbation of cell redox balance [1,2].Excessive productions of reactive oxygen species (ROS), such as O2 ́, OH and H2 O2, can cause base damage, strand breaks in DNA, as well as disruptions in normal mechanisms of cellular signaling [3,4].Endothelial dysfunction plays a key role in cardiovascular diseases
We investigated the ability of SAL to prevent cell injury of human umbilical vein study indicated that salidroside might be a functional chemopreventative agent that ameliorates endothelial cells (HUVECs) induced by oxidative stress
Results demonstrated that incubating HUVECs with SAL (0.1, 1, and 10 μM) for 24 h that incubating HUVECs with SAL (0.1, 1, and 10 μM) for 24 h antagonized the effects of 300 μM H2 O2 antagonized the effects of 300 μM H2O2 on cell viability, and pretreatment with 1 μM SAL increased on cell viability, and pretreatment with 1 μM SAL increased cell viability to 79.07% ̆ 3.13%, which was cell viability to 79.07% ± 3.13%, which was better than the others (Figure 2c)
Summary
Oxidative stress is defined as an excessive production of reactive oxygenated species that cannot be counteracted by the action of antioxidants, and as a perturbation of cell redox balance [1,2]. Salidroside (SAL, Figure 1), one of the main antioxidant activity, and inhibit the overproduction of pro-inflammatory cytokines through the effective constituents of Rhodiola rosea, possesses a wide range of pharmacological activities such as mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-κB) pathway [28]. We investigated the ability of SAL to prevent cell injury of human umbilical vein study indicated that salidroside might be a functional chemopreventative agent that ameliorates endothelial cells (HUVECs) induced by oxidative stress. It was demonstrated that salidroside exerts angiogenic expression of Nrf, HO-1, NQO1 and nuclear translocation of Nrf were evaluated to clarify the and cytoprotective effects on human bone marrow-derived endothelial progenitor cells via Akt/. Incubation with 0.1–10 μM SAL for 24 h didn’t affect cell viability, whereas higher
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