Icariin Attenuates High Glucose-Induced Apoptosis, Oxidative Stress, and Inflammation in Human Umbilical Venous Endothelial Cells

Sun, Si; Liu, Le; Tian, Xiaojun; Guo, Yanghongyun; Mei, Yunqing; Wang, Changhua

doi:10.1055/a-0837-0975

“…High glucose treatment was performed as our described previously [29,30]. The control group received the treatment of 5.5 mM glucose and the identical concentration of mannitol which act as osmotic control to remove a hyperosmolar effect.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Heat shock protein 60 (HSP60) modulates adiponectin signaling by stabilizing adiponectin receptor

Zhang

¹

,

Liu

²

,

Zhang

³

et al. 2020

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Adiponectin, an adipokine produced and secreted by adipocytes, is involved in regulating the development and progression of insulin resistance, diabetes, and diabetic complications. Heat shock protein 60 (HSP60) is a molecular chaperone, most commonly presenting in mitochondria and participating in the maintenance of protein homeostasis. Accumulating studies have demonstrated that the elevated circulating HSP60 and the decreased intracellular HSP60 are closely associated with diabetic complications such as diabetic cardiomyopathy. However, the underlying mechanism remains poorly understood. In the present study, we reported that HSP60 interacted directly with adiponectin receptors. Its abundance was positively associated with adiponectin action. Furthermore, HSP60 depletion markedly mitigated the protective impacts of adiponectin on high glucose-induced oxidative stress and cell apoptosis in rat cardiac H9c2 cells. In addition, HSP60 knockdown significantly enhanced proteasome activity leading to the degradation of adiponectin receptor 1. Taken together, we showed for the first time that HSP60 interacted with adiponectin receptors and mediated adiponectin signaling through stabilizing adiponectin receptor. This in vitro study also provides an alternative explanation for mechanism by which adiponectin exerts its action.

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“…High glucose treatment was performed as our described previously [20,21]. The control group received the treatment of 5.5 mM glucose and the identical concentration of mannitol which act as osmotic control to remove a hyperosmolar effect.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Heat shock protein 60 (HSP60) modulates adiponectin signaling by stabilizing adiponectin receptor

Zhang

¹

,

Liu

²

,

Zhang

³

et al. 2019

Preprint

Self Cite

View full text Add to dashboard Cite

Adiponectin, an adipokine produced and secreted by adipocytes, is involved in regulating the development and progression of insulin resistance, diabetes, and diabetic complications. Heat shock protein 60 (HSP60) is a molecular chaperone, most commonly presenting in mitochondria and participating in the maintenance of protein homeostasis. Accumulating studies have demonstrated that the elevated circulating HSP60 and the decreased intracellular HSP60 are closely associated with diabetic complications such as diabetic cardiomyopathy. However, the underlying mechanism remains poorly understood. In the present study, we reported that HSP60 interacted directly with adiponectin receptors. Its abundance was positively associated with adiponectin action. Furthermore, HSP60 depletion markedly mitigated the protective impacts of adiponectin on high glucose-induced oxidative stress and cell apoptosis in rat cardiac H9c2 cells. In addition, HSP60 knockdown significantly enhanced proteasome activity leading to the degradation of adiponectin receptor 1. Taken together, we showed for the first time that HSP60 interacted with adiponectin receptors and mediated adiponectin signaling through stabilizing adiponectin receptor. This in vitro study also provides an alternative explanation for mechanism by which adiponectin exerts its action.

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“…Effective herbal drugs for treatment of endothelial dysfunction should be able to improve NO synthesis and reduce ROS synthesis and apoptosis induced by deleterious agents such as high concentration of d -glucose or hydrogen peroxide [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…The authors found that the polyphenolic compounds in the extract were potent ROS inhibitors, capable of blocking protein glycation, and had an antiapoptotic effect. Recently, it has been determined that icariin, a flavonoid glycoside isolated from the plant species Epimedium , can protect against high d -glucose-induced endothelial dysfunction in vitro, through attenuation of apoptosis, oxidative stress, and inflammation [ 18 ]. In general, HUVECs are considered a reliable and simple in vitro model for predicting and understanding the biological response of endothelial cells to plant extracts.…”

Section: Introductionmentioning

confidence: 99%

Improvement of endothelial function by Gunnera tinctoria extract with antioxidant properties

Sabando¹,

Rodríguez-Díaz

²

,

Ide³

et al. 2020

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Background Gunnera tinctoria has been collected by Mapuche-Pewenche people for food and medicinal purposes. The high polyphenol content of methanolic extract from G. tinctoria leaves with chemical constituents such as ellagic acid and quercetin derivatives suggests its application to prevent endothelial dysfunction and oxidative stress. The aim of this study was to provide evidence of the protective effect of this extract on endothelial function by reducing oxidative stress induced by high d-glucose and H2O2, as well as by stimulating nitric oxide (NO) levels in human umbilical vein endothelial cells (HUVECs). Results A methanolic extract with a high content of polyphenols (520 ± 30 mg gallic acid equivalents/g dry extract) was obtained from G. tinctoria leaves. Its main constituent was ellagic acid. The results of Ferric reducing antioxidant power and 2,2-diphenyl-1-picrylhydrazyl radical scavenging assays of the extract confirmed its antioxidant activity by inhibition pathway of radical species. The incubation of HUVECs with the extract decreased the apoptosis and reactive oxygen species (ROS) synthesis induced by high extracellular concentration of d-glucose or hydrogen peroxide. The extract increased endothelial NO levels and reduced vasoconstriction in human placental vessels. Conclusions This study provides evidence about the antioxidant and endothelial protective properties of methanolic G. tinctoria leaf extract. The extract improves the availability of NO in HUVECs, inhibiting the production of ROS and vasoconstriction.

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Icariin Attenuates High Glucose-Induced Apoptosis, Oxidative Stress, and Inflammation in Human Umbilical Venous Endothelial Cells

Cited by 27 publications

References 58 publications

Heat shock protein 60 (HSP60) modulates adiponectin signaling by stabilizing adiponectin receptor

Heat shock protein 60 (HSP60) modulates adiponectin signaling by stabilizing adiponectin receptor

Heat shock protein 60 (HSP60) modulates adiponectin signaling by stabilizing adiponectin receptor

Improvement of endothelial function by Gunnera tinctoria extract with antioxidant properties

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