<i>Retracted:</i> Effects of astragalus polysaccharide on apoptosis of myocardial microvascular endothelial cells in rats undergoing hypoxia/reoxygenation by mediation of the PI3K/Akt/eNOS signaling pathway

Zhou, Qingling; Meng, Guowei; Teng, Fei; Sun, Qiang; Zhang, Yongshan

doi:10.1002/jcb.26243

Cited by 23 publications

(17 citation statements)

References 29 publications

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“…PI3K/Akt signaling is shown to play a protective role in myocardial ischemia-reperfusion. [17][18][19] Interestingly, a recent study reported that Notch signaling acted upstream of Akt to mediate the protective effects of oncostatin M on myocardial ischemia/reperfusion injury. 20 In addition, our previous study showed that Hes1 downregulated the expression of PTEN and promoted the phosphorylation of Akt in cardiac myocytes exposed to H/R, leading to improved cell survival.…”

Section: Discussionmentioning

confidence: 99%

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction

Zhou

Zhu

Liu

et al. 2018

J of Cellular Biochemistry

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Currently, the role of Notch signaling during myocardial infarction (MI) remains controversy. In this study we used in vitro and in vivo approaches to investigate the role of Notch signaling in MI. Using cultured human umbilical vein endothelial cells exposed to hypoxia/reoxygenation (H/R), we demonstrated that H/R inhibited the proliferation, VEGF secretion, and tube formation of HUVECs, and these effects were correlated with the inhibition of Notch signaling. Furthermore, these effects were antagonized by overexpression of NICD but aggravated by knockdown of NICD. In addition, in MI model rats we found that heart dysfunction and angiogenesis in model rats was partly improved by NICD overexpression but was aggravated by knockdown of NICD. In conclusion, these data demonstrate that Notch signaling is downregulated in H/R injury in the hearts. Artificial activation of Notch signaling could promote myocardial survival and angiogenesis and improve cardiac function following H/R injury.

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Section: Discussionmentioning

confidence: 99%

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction

Zhou

Zhu

Liu

et al. 2018

J of Cellular Biochemistry

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“…The results from the present study supported this finding and clarified that pretreatment with XNJ reduced these changes in rat cerebral tissue. Endothelial NO synthase (eNOS) has been proved to play a critical role in proliferation and apoptosis by suppressing the proapoptotic proteins [ 27 , 28 ]. NO produced by eNOS is considered to be a protective event against brain I/R injury [ 29 – 31 ].…”

Section: Discussionmentioning

confidence: 99%

Xingnaojing Injection Protects against Cerebral Ischemia Reperfusion Injury via PI3K/Akt‐Mediated eNOS Phosphorylation

Zhang

Zhai

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Xingnaojing (XNJ) injection, derived from traditional Chinese medicine formulation, has a protective effect against stroke, but the underlying mechanism is unclear, which severely limited its clinical application. This research aims to elucidate the role and mechanism of XNJ in reducing cerebral ischemic reperfusion (I/R) injury. Rats received 2 h cerebral ischemia followed by reperfusion of 24 h and were intraperitoneally given 5, 10, or 15 ml/kg XNJ 24 h before ischemia and at the onset of reperfusion, respectively. TTC staining, HE staining, and neurological score were implied to evaluate the effectiveness of XNJ. The protein expressions of PI3K/Akt and eNOS signaling were measured. Experiments were further performed in human brain microvascular endothelial cells (HBMECs) to investigate the protective mechanisms of XNJ. HBMECs were subjected to 3 h oxygen and glucose deprivation following 24 h of reoxygenation (OGD) to mimic cerebral I/R in vitro. PI3K inhibitor LY294002 was added with or without the preconditioning of XNJ. Multiple methods including western blot, immunofluorescence, DAPI staining, JC-1, and flow cytometry were carried out to evaluate the effect of XNJ on HBMECs. XNJ could improve rat cerebral ischemic injury and OGD induced HBMECs apoptosis. In vivo and in vitro researches indicated that the mechanism might be relevant to the activation of PI3K/Akt/eNOS signaling.

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“…H/R is an accepted and ideal in vitro model mimicking I/R injury [ 21 ]. It was reported that endothelial cells are very vulnerable to I/R and H/R injury [ 7 , 22 ]. In the present study, we found that H/R exposure significantly induced apoptosis of cultured HAECs, resulting in the dramatic inhibition of cell viability.…”

Section: Discussionmentioning

confidence: 99%

Baicalin Suppresses Hypoxia-Reoxygenation-Induced Arterial Endothelial Cell Apoptosis via Suppressing PKCδ/p53 Signaling

et al. 2017

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BackgroundThis study was aimed to investigate the protective role of baicalin on vascular endothelium exposed to ischemia reperfusion injury and the involved molecular mechanisms.Material/MethodsCultured human arterial endothelial cells (HAECs) were exposed to hypoxia/deoxygenation (H/R). Cells were also treated with baicalin at serially diluted concentrations. Cells were also treated with PKC activator PEP005 or specific siRNA against protein kinase Cδ (PKCδ). MTT assay was used to evaluate the cell viabilities. Flow cytometry was used to detect cell apoptosis. The protein phosphorylation and expression levels were determined by Western blotting.ResultsPKCδ-siRNA transfection increased cell viabilities and reduced cell apoptosis in HAECs exposed to H/R. Baicalin treatment preserved cell viabilities and reduced apoptosis of H/R-exposed HAECs in a concentration-dependent manner. Baicalin treatment reduced phosphorylation levels of PKCδ and p53, as well as the expression levels of active caspase3 and bax in HAECs exposed to H/R. The treatment of PKC activator PEP005 impaired the protective effects of baicalin in increasing cell viabilities and reducing apoptosis in HAECs exposed to H/R.ConclusionsBaicalin exerts vascular a protective effect on HAECs exposed to H/R by reducing cell apoptosis. The PKCδ/p53 apoptotic signaling pathway was the pharmacological target of baicalin.

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Retracted: Effects of astragalus polysaccharide on apoptosis of myocardial microvascular endothelial cells in rats undergoing hypoxia/reoxygenation by mediation of the PI3K/Akt/eNOS signaling pathway

Abstract: The study explores the effect of astragalus polysaccharide (APS) mediating P13K/ Akt/eNOS signaling pathway on apoptosis of myocardial microvascular endothelial cells (MMECs) in hypoxia/reoxygenation

Cited by 23 publications

References 29 publications

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction

Xingnaojing Injection Protects against Cerebral Ischemia Reperfusion Injury via PI3K/Akt‐Mediated eNOS Phosphorylation

Baicalin Suppresses Hypoxia-Reoxygenation-Induced Arterial Endothelial Cell Apoptosis via Suppressing PKCδ/p53 Signaling

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