Protective effect of tert-butylhydroquinone on cerebral inflammatory response following traumatic brain injury in mice

Jin, Wei; Kong, Jie; Handong, Wang; Wu, Jun; Lu, Tianyu; Jiang, Jian; Ni, Hongbin; Liang, Wei

doi:10.1016/j.injury.2011.03.009

Cited by 54 publications

(40 citation statements)

References 33 publications

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“…Cell death and neurodegeneration after TBI occur not only because of the first impact, but also from secondary brain injury [45, 48]. Our data showed that EC reduced water content at 3 days post-TBI and lessened cell and neuronal death (as evidenced by a reduction in PI and FJB staining), while increasing neuronal survival (as shown by stereological analysis of Cresyl violet-stained neurons).…”

Section: Discussionmentioning

confidence: 50%

Cerebroprotection of flavanol (-)-epicatechin after traumatic brain injury via Nrf2-dependent and -independent pathways

Tian

Wang

et al. 2016

Free Radical Biology and Medicine

109

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Traumatic brain injury (TBI), which leads to disability, dysfunction, and even death, is a prominent health problem worldwide with no effective treatment. A brain-permeable flavonoid named (−)-epicatechin (EC) modulates redox/oxidative stress and has been shown to be beneficial for vascular and cognitive function in humans and for ischemic and hemorrhagic stroke in rodents. Here we examined whether EC is able to protect the brain against TBI-induced brain injury in mice and if so, whether it exerts neuroprotection by modulating the NF-E2-related factor (Nrf2) pathway. We used the controlled cortical impact model to mimic TBI. EC was administered orally at 3 h after TBI and then every 24 h for either 3 or 7 days. We evaluated lesion volume, brain edema, white matter injury, neurologic deficits, cognitive performance and emotion-like behaviors, neutrophil infiltration, reactive oxygen species (ROS), and a variety of injury-related protein markers. Nrf2 knockout mice were used to determine the role of the Nrf2 signaling pathway after EC treatment. In wild-type mice, EC significantly reduced lesion volume, edema, and cell death and improved neurologic function on days 3 and 28; cognitive performance and depression-like behaviors were also improved with EC administration. In addition, EC reduced white matter injury, heme oxygenase-1 expression, and ferric iron deposition after TBI. These changes were accompanied by attenuation of neutrophil infiltration and oxidative insults, reduced activity of matrix metalloproteinase 9, decreased Keap 1 expression, increased Nrf2 nuclear accumulation, and increased expression of superoxide dismutase 1 and quinone 1. However, EC did not significantly reduce lesion volume or improve neurologic deficits in Nrf2 knockout mice after TBI. Our results show that EC protects the TBI brain by activating the Nrf2 pathway, inhibiting heme oxygenase-1 protein expression, and reducing iron deposition. The latter two effects could represent an Nrf2-independent mechanism in this model of TBI.

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Section: Discussionmentioning

confidence: 50%

Cerebroprotection of flavanol (-)-epicatechin after traumatic brain injury via Nrf2-dependent and -independent pathways

Tian

Wang

et al. 2016

Free Radical Biology and Medicine

109

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“…Oral administration of tBHQ prevented glomerular injury in diabetic mice (Li et al, 2011). Moreover, pre-treatment with tBHQ also protected mice brains against traumatic brain injury-induced inflammatory damage (Jin et al, 2011). In the present study, deterioration of the seminiferous epithelium and loose interstitial cells were evident.…”

Section: Discussionsupporting

confidence: 58%

Preventive effect of tert-butylhydroquinone on scrotal heat-induced damage in mouse testes

Li¹,

Piao²,

Nagaoka³

et al. 2013

Genet. Mol. Res.

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ABSTRACT.To investigate the effect of tert-butylhydroquinone (tBHQ) on scrotal heat-induced damage in mice testes, 8-week-old mice were divided into 6 groups and administered with or without tBHQ through diet (10 mg/g), intraperitoneal injection (100 mg/ kg body weight), or intratestis injection (12.5 mg/kg body weight), respectively. After single scrotal heat exposure (42°C for 25 min), trunk blood and testes were collected 48 h later. The testes from diet and intraperitoneal tBHQ-treated mice showed more compact interstitial cells and less germ cell loss in the seminiferous epithelium compared with their corresponding non-tBHQ groups. However, intratestis tBHQ treatment showed no marked difference relative to the non-treatment group. In addition, pre-treatment of tBHQ caused lower testosterone concentrations and reduced expression of cytochrome P450 17α-hydroxylase/17,20-lyase (CYP 17) compared to the corresponding non-tBHQ groups. The results indicated that scrotal heat-induced structural damage was partly prevented by pretreatment of tBHQ, which could be used as an effective antioxidant for preventing scrotal heat-mediated male infertility.

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“…Treatment with sulforaphane further increased the expression of Nrf2, HO-1, NQ01 and glutathione S-transferase-α1 (GST-α1) resulting in the reduction of brain edema, cortical neuronal death and motor deficits [132]. Tert-butylhydroquinone, another activator of Nrf2 protects against TBI-induced inflammation and damage via reduction in NF-KB activation and TNFα and IL-1β production following injury in the mouse closed head injury model [133]. Collectively these studies demonstrate a significant neuroprotective role of Nrf2 signaling through the activation of antioxidant enzymes and reduction of the inflammatory secondary injury response following CNS injury.…”

Section: Recent Advances In Antioxidant Therapeutic Strategiesmentioning

confidence: 99%

Antioxidant therapies in traumatic brain and spinal cord injury

Bains

Hall

2012

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

371

295

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Free radical formation and oxidative damage have been extensively investigated and validated as important contributors to the pathophysiology of acute central nervous system injury. The generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is an early event following injury occurring within minutes of mechanical impact. A key component in this event is peroxynitrite-induced lipid peroxidation. As discussed in this review, peroxynitrite formation and lipid peroxidation irreversibly damages neuronal membrane lipids and protein function, which results in subsequent disruptions in ion homeostasis, glutamate-mediated excitotoxicity, mitochondrial respiratory failure and microvascular damage. Antioxidant approaches include the inhibition and/or scavenging of superoxide, peroxynitrite, or carbonyl compounds, the inhibition of lipid peroxidation and the targeting of the endogenous antioxidant defense system. This review covers the preclinical and clinical literature supporting the role of ROS and RNS and their derived oxygen free radicals in the secondary injury response following acute traumatic brain injury (TBI) and spinal cord injury (SCI) and reviews the past and current trends in the development of antioxidant therapeutic strategies. Combinatorial treatment with the suggested mechanistically complementary antioxidants will also be discussed as a promising neuroprotective approach in TBI and SCI therapeutic research. This article is part of a Special Issue entitled: Antioxidants and antioxidant treatment in disease.

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Protective effect of tert-butylhydroquinone on cerebral inflammatory response following traumatic brain injury in mice

Cited by 54 publications

References 33 publications

Cerebroprotection of flavanol (-)-epicatechin after traumatic brain injury via Nrf2-dependent and -independent pathways

Cerebroprotection of flavanol (-)-epicatechin after traumatic brain injury via Nrf2-dependent and -independent pathways

Preventive effect of tert-butylhydroquinone on scrotal heat-induced damage in mouse testes

Antioxidant therapies in traumatic brain and spinal cord injury

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