Protective effect of ultrafiltered XinMaiJia extract against H2O2-induced injury in human umbilical vein endothelial cells through NHE1 downregulation

Yin, Yulong; Li, P.; Yang, Junyao; Liu, D.W.; Sun, Ruili; Pan, Guopin; Wan, Guo; Wan, Guoguo

doi:10.4238/2014.october.20.20

Cited by 5 publications

(6 citation statements)

References 17 publications

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“…Once generated, ROS readily react with unsaturated fatty acids and cholesterol molecules present in cell membranes, thus leading to cellular apoptosis through mitochondrial pathways involving nuclear factor-κB, p53 and stress-activated protein kinase ( 41 ). In the present study, oxidative stress was investigated in HUVECs by assessing ROS production and MDA concentration; the results of which revealed that ROS and MDA levels were significantly increased following H 2 O 2 treatment, whereas cell viability was significantly reduced, thus indicating that H 2 O 2 was able to induced apoptosis in HUVECs, which is in accordance with previous studies ( 27 , 37 ).…”

Section: Discussionsupporting

confidence: 90%

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Roles of miR-4463 in H2O2-induced oxidative stress in human umbilical vein endothelial cells

Wang¹,

He²,

Deng³

et al. 2017

Molecular Medicine Reports

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Oxidative stress is implicated in the pathophysiology of vascular diseases, including atherosclerosis, aneurysm and arteriovenous fistula. A previous study from our lab suggested that microRNA (miR)-4463 may be involved in the pathogenesis of vascular disease; however, the roles of oxidative stress in the molecular mechanisms underlying the actions of miR-4463 in vascular disease have yet to be elucidated. The aim of the present study was to investigate the role of miR-4463 in hydrogen peroxide (H2O2)-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). Reverse transcription-quantitative polymerase chain reaction was used to assess the expression levels of miR-4463 in HUVECs treated with various concentrations of H2O2. Flow cytometry was used to evaluate the percentage of apoptotic cells, and the protein expression levels of the apoptotic markers cleaved (C)-caspase3, poly (adenosine diphosphate-ribose) polymerase 1 (PARP1), B cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax) and X-linked inhibitor of apoptosis protein (XIAP) were determined using western blot analysis. The results demonstrated that the apoptotic rate of HUVECs was increased following treatment with H2O2 in a concentration-dependent manner, and the expression of miR-4463 was also upregulated in a dose-dependent manner. Following transfection with miR-4463 mimics, the levels of malondialdehyde and reactive oxygen species were increased in HUVECs, with a corresponding increase in the apoptotic rate. Furthermore, western blot analysis revealed that the protein expression levels of C-caspase3, PARP1 and Bax were upregulated, whereas the levels of Bcl-2 and XIAP were downregulated. In conclusion, the present findings suggested that the upregulation of miR-4463 may enhance H2O2-induced oxidative stress and promote apoptosis in HUVECs in vitro.

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Section: Discussionsupporting

confidence: 90%

“…3 ). Annexin V-positive cells and cellular uptake of PI were evaluated in order to distinguish between living, apoptotic and necrotic cells, as previously described ( 37 ). The proapoptotic effects of H 2 O 2 treatment appeared to be concentration-dependent ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Roles of miR-4463 in H2O2-induced oxidative stress in human umbilical vein endothelial cells

Wang¹,

He²,

Deng³

et al. 2017

Molecular Medicine Reports

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“…By using gene expression array, we identified several signaling pathways related to NO, FOXO, apoptosis, cell cycle, AMPK, MAPK, NF-kB, and PPAR, which were affected by XMJ in endothelial cells. We choose NO signaling as a candidate because NO signaling was in the pecking order among these signaling, consistent with our previous studies that XMJ produces the anti-inflammatory and antioxidant effects in HUVECs by increasing NO productions 19 26 27 . This is also highly related to clinical investigations that Chinese medicine has globally recognized to improve health conditions by activating NO signaling 28 .…”

Section: Discussionmentioning

confidence: 91%

Traditional Chinese medicine xin-mai-jia recouples endothelial nitric oxide synthase to prevent atherosclerosis in vivo

Yin

Zhu

Wan

et al. 2017

Sci Rep

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Endothelial dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial step in atherosclerosis. This study was designed to explore whether Chinese medicine xin-mai-jia (XMJ) recouples eNOS to exert anti-atherosclerotic effects. Pretreatment of XMJ (25, 50, 100 μg/ml) for 30 minutes concentration-dependently activated eNOS, improved cell viabilities, increased NO generations, and reduced ROS productions in human umbilical vein endothelial cells incubated with H2O2 for 2 hours, accompanied with restoration of BH4. Importantly, these protective effects produced by XMJ were abolished by eNOS inhibitor L-NAME or specific eNOS siRNA in H2O2-treated cells. In ex vivo experiments, exposure of isolated aortic rings from rats to H2O2 for 6 hours dramatically impaired acetylcholine-induced vasorelaxation, reduced NO levels and increased ROS productions, which were ablated by XMJ in concentration-dependent manner. In vivo analysis indicated that administration of XMJ (0.6, 2.0, 6.0 g/kg/d) for 12 weeks remarkably recoupled eNOS and reduced the size of carotid atherosclerotic plaque in rats feeding with high fat diet plus balloon injury. In conclusion, XMJ recouples eNOS to prevent the growth of atherosclerosis in rats. Clinically, XMJ is potentially considered as a medicine to treat patients with atherosclerosis.

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“…Development of pathological oxidative stress injury participates in this disease. Currently, many studies have considered the H 2 O 2 -induced cell injury model as the model by which to elucidate mechanisms related to neuroinflammation and apoptosis-linked cell injury in vitro and its treatment outcomes, [42][43][44][45][46] because H 2 O 2 simulate hypoxic environments, including, ROS production and loss of MMP in neuron. Protection of DNLA against ischemia-induced injury in vivo has been reported.…”

Section: Discussionmentioning

confidence: 99%

Dendrobium nobile Alkaloids Protects against H2O2-Induced Neuronal Injury by Suppressing JAK–STATs Pathway Activation in N2A Cells

Liu

Zhu

Niu

et al. 2020

Biological & Pharmaceutical Bulletin

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The purpose of this study was to investigate the preventive effect and mechanism of Dendrobium alkaloids (DNLA) on oxidative stress-related death in neuronal cells. Our results demonstrated that DNLA has a direct neuroprotective effect through oxidative stress in N2A cells induced by hydrogen peroxide (H 2 O 2). CCK8, lactate dehydrogenase (LDH), intracellular Ca 2 , intracellular reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were used to evaluate the mechanism of DNLA neutralization by H 2 O 2-induced injury. Results presented in the paper indicate that treatment with DNLA (35 ng/mL) significantly attenuated decreases in cell viability, release of LDH, and apoptosis after H 2 O 2-induced neuronal injury. Furthermore, DNLA significantly reduced intracellular Ca 2 up-regulation, ROS production, and inhibited mitochondrial depolarization. Moreover, DNLA treatment significantly downregulated expressions of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, nitric oxide synthase, janus kinase-signal transducer and activators of transcription (JAK-STATs) signaling in N2A cells, all of which were H 2 O 2-induced. Taken together, our findings suggested that DNLA may inhibit the expression of pro-inflammatory and proapoptotic factors by blocking JAK-STATs signaling after oxidative stress injury. This research provides a potential experimental basis for further application of DNLA to prevent various human nervous system diseases caused by oxidative stress.

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Protective effect of ultrafiltered XinMaiJia extract against H2O2-induced injury in human umbilical vein endothelial cells through NHE1 downregulation

Cited by 5 publications

References 17 publications

Roles of miR-4463 in H2O2-induced oxidative stress in human umbilical vein endothelial cells

Roles of miR-4463 in H2O2-induced oxidative stress in human umbilical vein endothelial cells

Traditional Chinese medicine xin-mai-jia recouples endothelial nitric oxide synthase to prevent atherosclerosis in vivo

<i>Dendrobium nobile</i> Alkaloids Protects against H<sub>2</sub>O<sub>2</sub>-Induced Neuronal Injury by Suppressing JAK–STATs Pathway Activation in N2A Cells

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