Daphnetin protects hippocampal neurons from oxygen‐glucose deprivation–induced injury

Jin, Zhi; Duan, Bin; Pei, Jiwen; Wu, Songdi; Wei, Junli

doi:10.1002/jcb.27698

Cited by 23 publications

(16 citation statements)

References 21 publications

(60 reference statements)

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“…49,50 OGD results in ischemic neuronal damage through activation of autophagy, neuroinflammatory responses, and induction of apoptosis in the hippocampal neuron in vitro. 51 OGD-induced apoptotic cell death occurs by the inhibiting the PI3K/AKT and BDNF/TrkB pathways, 40,52 and the neuroprotective effects of both URB597 and VEGF-A may be dependent on the activities of these two pathways. We previously demonstrated that URB597 could improve chronic cerebral ischemia-induced neuronal degeneration and apoptosis via activating CB1R/ AKT signaling.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of VEGF-A Nanofiber Membrane and FAAH Inhibitor URB597 Against Oxygen–Glucose Deprivation-Induced Ischemic Neuronal Injury

Wang¹,

Jin²,

Zhao

et al. 2021

IJN

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Introduction Brain ischemia is a common neurological disorder worldwide that activates a cascade of pathophysiological events involving decreases in oxygen and glucose levels. Despite substantial efforts to explore its pathogenesis, the management of ischemic neuronal injury remains an enormous challenge. Accumulating evidence suggests that VEGF modified nanofiber (NF) materials and the fatty-acid amide hydrolase (FAAH) inhibitor URB597 exert an influence on alleviating ischemic brain damage. We aimed to further investigate their effects on primary hippocampal neurons, as well as the underlying mechanisms following oxygen–glucose deprivation (OGD). Methods Different layers of VEGF-A loaded polycaprolactone (PCL) nanofibrous membranes were first synthesized by using layer-by-layer (LBL) self-assembly of electrospinning methods. The physicochemical and biological properties of VEGF-A NF membranes, and their morphology, hydrophilicity, and controlled-release of VEGF-A were then estimated. Furthermore, the effects of VEGF-A NF and URB597 on OGD-induced mitochondrial oxidative stress, inflammatory responses, neuronal apoptosis, and endocannabinoid signaling components were assessed. Results The VEGF-A NF membrane and URB597 can not only promote hippocampal neuron adhesion and viability following OGD but also exhibited antioxidant/anti-inflammatory and mitochondrial membrane potential protection. The VEGF-A NF membrane and URB597 also inhibited OGD-induced cellular apoptosis through activating CB1R signaling. These results indicate that VEGF-A could be controlled-released by LBL self-assembled NF membranes. Discussion The VEGF-A NF membrane and URB597 displayed positive synergistic neuroprotective effects through the inhibition of mitochondrial oxidative stress and activation of CB1R/PI3K/AKT/BDNF signaling, suggesting that a VEGF-A loaded NF membrane and the FAAH inhibitor URB597 could be of therapeutic value in ischemic cerebrovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of VEGF-A Nanofiber Membrane and FAAH Inhibitor URB597 Against Oxygen–Glucose Deprivation-Induced Ischemic Neuronal Injury

Wang¹,

Jin²,

Zhao

et al. 2021

IJN

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“…Mechanistically, daphnetin positively upregulated Nrf2 while it inhibited the expression Keap1 in HG-stimulated MCs [135]. Zhi et al reported that daphnetin protected hippocampal neurons exposed to oxygen-glucose deprivation-induced injury against I/R via marked enhancement of the nuclear translocation of Nrf2 and HO-1 expression [136]. Moreover, Nrf2 knockdown blocked the protective effect of daphnetin on I/R in hippocampal neurons, confirming the critical role of Nrf2/HO-1 signaling activation in the neuroprotective effect of daphnetin [136].…”

Section: Urolithin Amentioning

confidence: 99%

“…Zhi et al reported that daphnetin protected hippocampal neurons exposed to oxygen-glucose deprivation-induced injury against I/R via marked enhancement of the nuclear translocation of Nrf2 and HO-1 expression [136]. Moreover, Nrf2 knockdown blocked the protective effect of daphnetin on I/R in hippocampal neurons, confirming the critical role of Nrf2/HO-1 signaling activation in the neuroprotective effect of daphnetin [136]. Lv and coworkers demonstrated that daphnetin effectively inhibited cytochrome c release and NLRP3 inflammasome activation through upregulation of the Nrf2 nuclear translocation along with Keap1 protein downregulation [137].…”

Section: Urolithin Amentioning

confidence: 99%

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Hassanein

Sayed

Hussein

et al. 2020

Oxidative Medicine and Cellular Longevity

157

106

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The Keap1/Nrf2/ARE system is a central defensive mechanism against oxidative stress which plays a key role in the pathogenesis and progression of many diseases. Nrf2 is a redox-sensitive transcription factor controlling a variety of downstream antioxidant and cytodefensive genes. Nrf2 has a powerful anti-inflammatory activity mediated via modulating NF-κB. Therefore, pharmacological activation of Nrf2 is a promising therapeutic strategy for the treatment/prevention of several diseases that are underlined by both oxidative stress and inflammation. Coumarins are natural products with promising pharmacological activities, including antioxidant, anticancer, antimicrobial, and anti-inflammatory efficacies. Coumarins are found in many plants, fungi, and bacteria and have been widely used as complementary and alternative medicines. Some coumarins have shown an ability to activate Nrf2 signaling in different cells and animal models. The present review compiles the research findings of seventeen coumarin derivatives of plant origin (imperatorin, visnagin, urolithin B, urolithin A, scopoletin, esculin, esculetin, umbelliferone, fraxetin, fraxin, daphnetin, anomalin, wedelolactone, glycycoumarin, osthole, hydrangenol, and isoimperatorin) as antioxidant and anti-inflammatory agents, emphasizing the role of Nrf2 activation in their pharmacological activities. Additionally, molecular docking simulations were utilized to investigate the potential binding mode of these coumarins with Keap1 as a strategy to disrupt Keap1/Nrf2 protein-protein interaction and activate Nrf2 signaling.

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“…IACUC A1027). All animals were cared for in accordance with the recommendations of the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health (28).…”

Section: Fundingmentioning

confidence: 99%

“…Liu et al (26) reported that DAP has some protective effects on severe acute pancreatitis in a rat model by inhibiting the expression of inflammatory cytokines. Subsequently, DAP was found to prevent and treat numerous diseases, including cerebral ischaemia/reperfusion injury, rheumatoid arthritis, colitis and endotoxin-induced lung injury, due to its powerful anti-inflammatory activities (24,(27)(28)(29)(30)(31)(32). At present, DAP is an anti-inflammatory agent used in some inflammation-related diseases (33)(34)(35).…”

Section: Introductionmentioning

confidence: 99%

Daphnetin suppresses experimental abdominal aortic aneurysms in mice via inhibition of aortic mural inflammation

Xie

Guan

et al. 2020

Exp Ther Med

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Rupture of abdominal aortic aneurysm (AAA) is a devastating event that can be prevented by inhibiting the growth of small aneurysms. Therapeutic strategies targeting certain events that promote the development of AAA must be developed, in order to alter the course of AAA. Chronic inflammation of the aortic mural is a major characteristic of AAA and is related to AAA formation, development and rupture. Daphnetin (DAP) is a coumarin derivative with anti-inflammatory properties that is extracted from Daphne odora var. However, the effect of DAP on AAA development remains unclear. The present study investigated the effect of DAP on the formation and development of experimental AAAs and its potential underlying mechanisms. A mice AAA model was established by intra-aortic infusion of porcine pancreatic elastase (PPE), and mice were intraperitoneally injected with DAP immediately after PPE infusion. The maximum diameter of the abdominal aorta was measured by ultrasound system, and aortic mural changes were investigated by Elastica van Gieson (EVG) staining and immunohistochemical staining. The results demonstrated that DAP significantly suppressed PPE-induced AAA formation and attenuated the depletion of aortic medial elastin and smooth muscle cells in the media of the aorta. Furthermore, the density of mural macrophages, T cells and B cells were significantly attenuated in DAP-treated AAA mice. In addition, treatment with DAP resulted in a significant reduction in mural neovessels. These findings indicated that DAP may limit the formation and progression of experimental aneurysms by inhibiting mural inflammation and angiogenesis. These data confirmed the translational potential of DAP inclinical AAA inhibition strategies.

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Daphnetin protects hippocampal neurons from oxygen‐glucose deprivation–induced injury

Cited by 23 publications

References 21 publications

Neuroprotective Effects of VEGF-A Nanofiber Membrane and FAAH Inhibitor URB597 Against Oxygen–Glucose Deprivation-Induced Ischemic Neuronal Injury

Neuroprotective Effects of VEGF-A Nanofiber Membrane and FAAH Inhibitor URB597 Against Oxygen–Glucose Deprivation-Induced Ischemic Neuronal Injury

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Daphnetin suppresses experimental abdominal aortic aneurysms in mice via inhibition of aortic mural inflammation

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