Vitexin reduces hypoxia–ischemia neonatal brain injury by the inhibition of HIF-1alpha in a rat pup model

Min, Jia-Wei; Hu, Jiang-Jian; He, Maoxian; Sánchez, Raúl Hernández; Huang, Wenxian; Liu, Yuqiang; Bsoul, Najeeb; Han, Song; Yin, Jun; Liu, Wanhong; He, Xiaohua; Peng, Biwen

doi:10.1016/j.neuropharm.2015.07.007

Cited by 71 publications

(49 citation statements)

References 90 publications

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“…In the present study, vitexin induced VEGF protein expression in sevoflurane-induced newborn rat or human neuroglioma cells. Min et al indicated that vitexin reduces hypoxia-ischemia neonatal brain injury through suppression of HIF-1α and VEGF expression (22). Choi et al reported that Vitexin has anti-metastatic potential in PC12 cells through HIF-1alpha inhibitor and VEGF expression (23).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

et al. 2018

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Abstract. Previous studies have demonstrated thatVitexin possesses antihypertensive, anti-inflammatory and potential anticancer effects. The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase-3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane-induced newborn rats. In addition, Vitexin pretreatment increased superoxide dismutase and glutathione peroxidase activity. Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF-1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated-p38 MAP kinase (p38) protein expression in sevoflurane-induced newborn rat. Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α-, VEGF-and p38-associated signaling pathways in newborn rats.

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Section: Discussionmentioning

confidence: 99%

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

et al. 2018

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“…The protocol was approved by the Committee on the Ethics of Animal Experiments of Wuhan University (China) (Permit Number: SCXK 2008-0004). Mouse HI was carried out according to a method described previously [13, 30]. Briefly, postnatal day (P9) C57BL/6 mice of both sexes were anesthetized by inhalation of diethyl ether.…”

Section: Methodsmentioning

confidence: 99%

“…Furthermore, it has been shown that the neuroprotective function of vitexin are closely associated with the inhibition of apoptosis and Ca 2+ overload in cultured cortical neurons [12]. Previous studies have also found that vitexin reduced hypoxia-ischemia neonatal brain damage in a rat pup model [13] and ischemia/reperfusion injury in adult mice [14]. Therefore, vitexin has the potential to explore the roles of CaMKII in vitro and in vivo .…”

Section: Introductionmentioning

confidence: 99%

Vitexin protects against hypoxic-ischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinase II and apoptosis signaling in the neonatal mouse brain

et al. 2017

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Neonatal hypoxic-ischemic is a major cause of death and disability in neonates. In this study, we suggest for the first time that pretreatment with vitexin may suppress a pro-apoptotic signaling pathway in hypoxic-ischemic neuronal injury in neonates by inhibition of the phosphorylation of Ca2+/Calmodulin-dependent protein kinase II. Here we found that vitexin pretreatment reduced brain infarct volume in a dose-dependent manner. In addition, vitexin decreased the number of TUNEL-positive cells and brain atrophy. Furthermore, vitexin improved neurobehavioral outcomes. Vitexin also reduced oxygen glucose deprivation-induced neuronal injury and calcium entry. Vitexin pretreatment increased the Bcl-2/Bax protein ratio and decreased phosphorylation of Ca2+/Calmodulin-dependent protein kinase II and NF-κB, cleaved caspase-3 protein expression 24 hours after injury. Our data indicate that pretreatment with vitexin protects against neonatal hypoxic-ischemic brain injury and thus has potential as a treatment for hypoxic-ischemic brain injury.

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“…Each part was weighed immediately after removal (wet weight) and again after drying in an oven at 105 °C for 24 h as previously described (Min et al, 2015). The percentage of water content was calculated as [(wet weight -dry weight)/wet weight] ×100%.…”

Section: Brain Water Contentmentioning

confidence: 99%

Hydrogen-rich saline mediates neuroprotection through the regulation of endoplasmic reticulum stress and autophagy under hypoxia-ischemia neonatal brain injury in mice

et al. 2016

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Vitexin reduces hypoxia–ischemia neonatal brain injury by the inhibition of HIF-1alpha in a rat pup model

Cited by 71 publications

References 90 publications

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway inï¿½vitro and in newborn rats

Vitexin protects against hypoxic-ischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinase II and apoptosis signaling in the neonatal mouse brain

Hydrogen-rich saline mediates neuroprotection through the regulation of endoplasmic reticulum stress and autophagy under hypoxia-ischemia neonatal brain injury in mice

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