Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Cui, Xiaolu; Song, Haiqing; Shi, Jie

doi:10.3892/etm.2017.4683

Cited by 26 publications

(21 citation statements)

References 34 publications

(43 reference statements)

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“…or 5–30 µM), via HO-1 over-expression, was neuroprotective in a rat model of focal ischemia [63] and in rat cerebellar granule neurons exposed to hemin [64]. In an experimental system of rat hypoxic-ischemic brain injury, curcumin (150 mg/kg per os for three days) overexpressed HO-1 with a mechanism related to Nrf2 nuclear translocation [65]. In addition, curcumin (1–100 µM) has been shown to up-regulate HO-1 and, through this mechanism, it prevents oxygen glucose deprivation-induced damage in rat brain microvascular endothelial cells, a model mimicking the blood–brain barrier (BBB) function [66].…”

Section: Curcumin Neuroprotection and The Ho/bvr Pathwaymentioning

confidence: 99%

Curcumin and Heme Oxygenase: Neuroprotection and Beyond

Mhillaj

Tarozzi

Pruccoli

et al. 2019

IJMS

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Curcumin is a natural polyphenol component of Curcuma longa Linn, which is currently considered one of the most effective nutritional antioxidants for counteracting free radical-related diseases. Several experimental data have highlighted the pleiotropic neuroprotective effects of curcumin, due to its activity in multiple antioxidant and anti-inflammatory pathways involved in neurodegeneration. Although its poor systemic bioavailability after oral administration and low plasma concentrations represent restrictive factors for curcumin therapeutic efficacy, innovative delivery formulations have been developed in order to overwhelm these limitations. This review provides a summary of the main findings involving the heme oxygenase/biliverdin reductase system as a valid target in mediating the potential neuroprotective properties of curcumin. Furthermore, pharmacokinetic properties and concerns about curcumin’s safety profile have been addressed.

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Section: Curcumin Neuroprotection and The Ho/bvr Pathwaymentioning

confidence: 99%

Curcumin and Heme Oxygenase: Neuroprotection and Beyond

Mhillaj

Tarozzi

Pruccoli

et al. 2019

IJMS

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“…Curcumin, a low-molecular-weight bioactive compound isolated from turmeric (Curcuma longa), can affect various diseases by regulating oxidative stress, cell apoptosis, and the inflammatory response [14]. A recent study has suggested that curcumin can attenuate brain HI damage in neonatal rats [15]. However, whether curcumin improves brain HI damage via VEGF regulation is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Curcumin targets vascular endothelial growth factor via activating the PI3K/Akt signaling pathway and improves brain hypoxic-ischemic injury in neonatal rats

Wang

et al. 2020

Korean J Physiol Pharmacol

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This study aimed to evaluate the effect of curcumin on brain hypoxicischemic (HI) damage in neonatal rats and whether the phosphoinositide 3-kinase (PI3K)/Akt/vascular endothelial growth factor (VEGF) signaling pathway is involved. Brain HI damage models were established in neonatal rats, which received the following treatments: curcumin by intraperitoneal injection before injury, insulin-like growth factor 1 (IGF-1) by subcutaneous injection after injury, and VEGF by intracerebroventricular injection after injury. This was followed by neurological evaluation, hemodynamic measurements, histopathological assessment, TUNEL assay, flow cytometry, and western blotting to assess the expression of p-PI3K, PI3K, p-Akt, Akt, and VEGF. Compared with rats that underwent sham operation, rats with brain HI damage showed remarkably increased neurological deficits, reduced right blood flow volume, elevated blood viscosity and haematocrit, and aggravated cell damage and apoptosis; these injuries were significantly improved by curcumin pretreatment. Meanwhile, brain HI damage induced the overexpression of p-PI3K, p-Akt, and VEGF, while curcumin pretreatment inhibited the expression of these proteins. In addition, IGF-1 treatment rescued the curcumin-induced down-regulated expression of p-PI3K, p-Akt, and VEGF, and VEGF overexpression counteracted the inhibitory effect of curcumin on brain HI damage. Overall, pretreatment with curcumin protected against brain HI damage by targeting VEGF via the PI3K/Akt signaling pathway in neonatal rats.

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“…Previous reports showed that curcumin increases the expression of HO-1 [ 26 , 27 ]. We examined the expression of HO-1 in aortic tissue associated with curcumin-mixed HFD feed using the Western blot method.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies revealed that the expression of the anti-oxidative enzyme HO-1 increased, while curcumin suppresses acute hepatopathy and neonatal hypoxic-ischemic encephalopathy [ 26 , 27 ]. HO-1, one of the two HO isoforms, is expressed and induced in response to various stresses and produces CO of an equal moles to heme ratio, reduced iron (Fe 2+ ), and biliverdin by using protoheme IX, a prosthetic group of heme protein, as a substrate.…”

Section: Discussionmentioning

confidence: 99%

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Curcumin Inhibits Age-Related Vascular Changes in Aged Mice Fed a High-Fat Diet

et al. 2018

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Inhibiting the onset of arteriosclerotic disease, which has been increasing due to the westernized diet and aging, is a significant social challenge. Curcumin, a type of polyphenol, has anti-oxidative effects and anti-inflammatory action and is expected to treat and to have prophylactic effects on different diseases. In this study, we examined the effects of long-term administration of curcumin on vascular aging and chronic inflammation—the causes of arteriosclerotic disease. Eight-week-old C57BL/6J mice were fed with high fat diet (HFD) or 0.1% curcumin-mixed HFD (HFD + Cu) until 80 weeks old (n = 20 for each group). After the breeding, we examined the expression of antioxidant enzymes, heme oxygenase-1 (HO-1), oxidative stress, vascular aging, and inflammatory changes in the aorta. In the HFD group, oxidative stress increased with decreased sirt1 expression in the aorta followed by increased senescent cells and enhanced inflammation. Whereas in the HFD + Cu group, HO-1 was induced in the aorta with the suppression of oxidative stress. Additionally, it was shown that sirt1 expression in the aorta in the HFD + Cu group remained at a level comparable to that of the 8-week-old mice with suppression of increased senescent cells and enhanced inflammation. Consequently, disorders associated with HFD were resolved. These results suggest that curcumin might be a food with a prophylactic function against arteriosclerotic disease.

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Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Cited by 26 publications

References 34 publications

Curcumin and Heme Oxygenase: Neuroprotection and Beyond

Curcumin and Heme Oxygenase: Neuroprotection and Beyond

Curcumin targets vascular endothelial growth factor via activating the PI3K/Akt signaling pathway and improves brain hypoxic-ischemic injury in neonatal rats

Curcumin Inhibits Age-Related Vascular Changes in Aged Mice Fed a High-Fat Diet

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