Luteolin provides neuroprotection in models of traumatic brain injury via the Nrf2–ARE pathway

Xu, Jianguo; Ding, Ke; Zhang, Li; Wang, Handong; Li, Tao; Wei, Wen Jun; Lu, Xinyu

doi:10.1016/j.freeradbiomed.2014.03.009

Cited by 146 publications

(115 citation statements)

References 48 publications

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“…Previous studies have found that expression of Nrf2 begins to increase 2 h after traumatic brain injury, and its expression peaks after 24 h. Nrf2 expression then gradually decreases and returns to normal levels 3 to 5 days later (Cheng et al, 2013). The degree of traumatic brain injury in Nrf2 knockout mice is significantly more severe compared to wild type mice, and administration of drugs that up-regulate Nrf2 protein expression significantly reduces apoptosis of neurons and improves neurological function after traumatic brain injury Xie et al, 2014;Xu et al, 2014). Therefore, these results demonstrate that Nrf2 is a participant in secondary brain injury after traumatic brain injury, and regulation of the Nrf2 signaling pathway increases the levels of downstream antioxidants and detoxification enzymes, thereby contributing to neuroprotection.…”

Section: Discussionmentioning

confidence: 99%

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Meng¹,

Zhang²,

Li³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We investigated the effects of hyperbaric oxygen treatment on the Nrf2 signaling pathway in secondary injury following traumatic brain injury, using a rat model. An improved Feeney freefall method was used to establish the rat traumatic brain injury model. Sixty rats were randomly divided into three groups: a sham surgery group, a traumatic brain injury group, and a group receiving hyperbaric oxygen treatment after traumatic brain injury. Neurological function scores were assessed at 12 and 24 h after injury. The expression levels of Nrf2, heme oxygenase 1 (HO-1), and quinine oxidoreductase 1 (NQO-1) in the cortex surrounding the brain lesion were detected by western blotting 24 h after the injury. Additionally, the TUNEL method was used to detect apoptosis of nerve cells 24 h after traumatic injury and Nissl staining was used to detect the number of whole neurons. Hyperbaric oxygen treatment significantly increased the expression of nuclear Nrf2 protein (P < 0.05), HO-1, and NQO-1 in the brain tissues surrounding the lesion after a traumatic brain injury (P < 0.05) and also significantly reduced the number of apoptotic and injured nerve cells. The neurological function scores also improved with hyperbaric oxygen treatment (P < 0.05). Therefore, hyperbaric oxygen has a neuroprotective role in traumatic brain injury, which is mediated by up-regulation of the Nrf2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Meng¹,

Zhang²,

Li³

et al. 2016

Genet. Mol. Res.

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“…Neurological deficit was evaluated by the grip test, which was based on the test of gross vestibulomotor function as described elsewhere [8]. …”

Section: Methodsmentioning

confidence: 99%

Rutin Acid Ameliorates Neural Apoptosis Induced by Traumatic Brain Injury via Mitochondrial Pathways in Mice

Zhai

Ding

Wang

et al. 2016

Neuroimmunomodulation

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Rutin reportedly conveys many beneficial effects, including neuroprotection in brain injury. However, the mechanisms underlying these effects are still not well understood. This study investigates the effect of rutin on potential mechanisms for neuroprotective effects, using the weight-drop model of traumatic brain injury (TBI) in male mice treated either with rutin or a vehicle via intraperitoneal injection 30 min after TBI. After euthanasia and 24 h after TBI, all mice were examined by tests, including neurologic scores, blood-brain barrier permeability, brain water content and neuronal cell death in the cerebral cortex. Results indicate that the levels of cytochrome c, malondialdehyde (MDA) and superoxide dismutase (SOD) were restored by rutin treatment. Rutin treatment resulted in the downregulation of caspase-3 expression in a reduced number of positive cells under terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, and also the improved survival of neurons. Furthermore, pretreatment levels of MDA were restored, while Bcl-2-associated X protein translocation to mitochondria and cytochrome c release into cytosol were reduced by rutin treatment. Our results demonstrate that rutin improves neurological outcome by protecting neural cells against apoptosis via mechanisms that involve the mitochondria following TBI.

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“…Luteolin and luteolin-7-O-glucoside modulated Nrf2/mitogen-activated protein kinase (MAPK) mediated the HO-1 signaling cascade in RAW 264.7 cells [76]. In wildtype mouse traumatic brain injury models, luteolin showed neuroprotective action by Nrf2/ARE pathway activation [77]. Luteolin inhibited tBHP-induced oxidative stress by increasing ERK2/ Nrf2/ARE signaling pathway activation and HO-1, glutamate cysteine ligase catalytic (GCLC), and glutamate cysteine ligase modifier (GCLM) subunit transcription in rat primary hepatocytes [78].…”

Section: Luteolinmentioning

confidence: 99%

Stress Response of Dietary Phytochemicals in a Hormetic Manner for Health and Longevity

Gezer¹

2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

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The stress responses observed in mammalian cells can be classified as heat shock response, unfolded protein response, autophagic response, deoxyribonucleic acid damage response, antioxidant response, and sirtuin response at the intracellular and molecular levels. Factors that strengthen the hemodynamic structure causing low-level molecular damage and activating one or several stress response pathways are called hormetins. Hormetins can be categorized as physical, physiological, biological, and nutritional hormetins. Nutritional hormetins provide an interesting, comprehensive research topic because of their effects on health and lifespan. Dietary phytochemicals, with their low-level stress-inducing effects, are potential nutritional hormetins. Resveratrol, curcumin, epicatechin, isothiocyanates, ferulic acid, and certain vitamin-minerals can induce a heat shock response, unfolded protein response, autophagic response, deoxyribonucleic acid damage response, antioxidant response, and sirtuin response causing the stimulation of kinases and transcription factors. Studies have shown that these phytochemicals are related to nuclear factor-erythroid 2, sirtuins, nuclear factor-kappa B, and heat shock response pathways. In this chapter, the stress response of dietary phytochemicals will be systematically examined in a hormetic manner for delay of age-related diseases, healthy aging, and longevity based on current data.

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Luteolin provides neuroprotection in models of traumatic brain injury via the Nrf2–ARE pathway

Cited by 146 publications

References 48 publications

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Rutin Acid Ameliorates Neural Apoptosis Induced by Traumatic Brain Injury via Mitochondrial Pathways in Mice

Stress Response of Dietary Phytochemicals in a Hormetic Manner for Health and Longevity

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