Inhibition of leukotriene B4 synthesis protects against early brain injury possibly via reducing the neutrophil-generated inflammatory response and oxidative stress after subarachnoid hemorrhage in rats

Ye, Zhen-Nan; Wu, Lingyun; Liu, Jingpeng; Chen, Qiang; Zhang, Xiangsheng; Lu, Yaxin; Zhou, Meifang; Li, Wei; Zhang, Zihuan; Xia, Dayong; Zhuang, Zong; Hang, Chun-Hua

doi:10.1016/j.bbr.2017.11.011

Cited by 21 publications

(23 citation statements)

References 52 publications

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“…Immunofluorescence staining was performed according to our previously published Protocols (Sun et al, 2014;Ye et al, 2018). Briefly, brain sections (6 µm) were first incubated with primary antibodies against p65 (1:200, 1:1000, cat.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

MiR-146a Ameliorates Hemoglobin-Induced Microglial Inflammatory Response via TLR4/IRAK1/TRAF6 Associated Pathways

et al. 2020

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Microglial activation and sustained inflammation in the brain can lead to neuronal damage. Hence, limiting microglial activation and brain inflammation is a good therapeutic strategy for inflammatory-associated central nervous disease. MiR-146a is a promising therapeutic microRNA, since it can negatively regulate the inflammatory response. We thus investigated the expression changes of miR-146a after experimental induction of a subarachnoid hemorrhage (SAH) in vivo and in vitro, and we assessed the anti-inflammatory effects of miR-146a in microglial cells in vitro. Primary microglial cells were preincubated with miR-146a before hemoglobin (Hb) treatment. The results indicated that miR-146a decreased gene expression of Hb-induced pro-inflammatory cytokines (TNF-α and IL-1β) and phenotype-related genes (iNOS and CD86) through IRAK1/TRAF6/NF-κB or MAPK signaling pathways, suggesting its pro-resolution activity in microglia. However, contrary to the LPS-induced microglia or macrophage activation model, we did not observe an elevation in miR-146a after activation. Overall, our findings demonstrated that miR-146a was involved in the regulation of brain inflammation and could be considered a novel therapeutic agent for treating brain inflammation.

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Section: Immunofluorescence Stainingmentioning

confidence: 99%

MiR-146a Ameliorates Hemoglobin-Induced Microglial Inflammatory Response via TLR4/IRAK1/TRAF6 Associated Pathways

et al. 2020

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“…After SAH, oxidative stress is implicated in the etiology of at all stages of SAH (early brain injury, cerebral vasospasm, and delayed cerebral ischemia) ( Ersahin et al, 2010 ; Zhang et al, 2015 ; Li et al, 2016 ; Ye et al, 2018 ). The high concentration of reactive oxygen species (ROS)/reactive nitrogen species (RNS) is considered to be associated with impaired cerebral autoregulation ( Choi et al, 2001 ; Shin et al, 2002 ) ( Figure 1 ).…”

Section: Cerebral Autoregulation Dysfunction After Sahmentioning

confidence: 99%

Antioxidant Melatonin: Potential Functions in Improving Cerebral Autoregulation After Subarachnoid Hemorrhage

et al. 2018

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Subarachnoid hemorrhage (SAH) is a subtype of stroke with high mortality and morbidity. Impaired cerebral autoregulation following SAH has been reported owing to effects on sympathetic control, endothelial function, myogenic response, and cerebral metabolism. Impaired cerebral autoregulation is associated with early brain injury, cerebral vasospasm/delayed cerebral ischemia, and SAH prognosis. However, few drugs have been reported to improve cerebral autoregulation after SAH. Melatonin is a powerful antioxidant that is effective (easily crosses the blood brain barrier) and safe (tolerated in large doses without toxicity). Theoretically, melatonin may impact the control mechanisms of cerebral autoregulation via antioxidative effects, protection of endothelial cell integrity, suppression of sympathetic nerve activity, increase in nitric oxide bioavailability, mediation of the myogenic response, and amelioration of hypoxemia. Furthermore, melatonin may have a comprehensive effect on cerebral autoregulation. This review discusses the potential effects of melatonin on cerebral autoregulation following SAH, in terms of the association between pharmacological activities and the mechanisms of cerebral autoregulation.

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“…(D) Expression of c-Myc (mean ± SD; n = 3; *p < 0.05). (Zhang et al, 2017;Ye et al, 2018). It has been reported that the inactivation of Wnt/b-catenin signaling is associated with neuronal apoptosis (Takadera et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Subarachnoid hemorrhage (SAH), which accounts for 5% of all stroke cases, is a severe neurological disorder with extremely high rates of mortality and morbidity (Boettinger et al, 2017;Ye et al, 2018). The causes of SAH are rupture of intracranial aneurysm and severe craniocerebral injury (Anzabi et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…The general assumption is that EBI induced by a decrease in cerebral blood flow is the primary cause of poor prognosis and plays an important role in the overall outcome (Feng et al, 2016). Neuronal apoptosis, which induces disruption of the blood-brain barrier, oxidative stress, brain edema, and elevated intracranial pressure, is a common result of general EBI (Ye et al, 2018). However, the exact molecular mechanisms underlying neuronal apoptosis have not been fully studied.…”

Section: Introductionmentioning

confidence: 99%

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Propoxyphene Mediates Oxyhemoglobin-Induced Injury in Rat Cortical Neurons Through Up-Regulation of Active-β-Catenin

Wang

et al. 2020

Front. Pharmacol.

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Wnt/b-catenin signaling is involved in various biological processes, including the development of the central nervous system. The dysfunction of mitochondria has been shown to participate in the progress of subarachnoid hemorrhage (SAH). Traumatic subarachnoid hemorrhage (tSAH) is a serious complication in acute craniocerebral trauma. Opioids can activate the canonical Wnt/b-catenin signaling pathway. c-Myc, a downstream protein of Wnt/b-catenin signaling, contributes to the fusion of mitochondria. Here, we investigated the protective roles of Propoxyphene (Pro) against Oxyhemoglobin (OxyHb)-induced primary cultured neuron apoptosis. The data indicated that Pro rescued active-b-catenin from OxyHb-induced decline. Furthermore, Pro attenuated OxyHbinduced apoptosis and fission of mitochondria in primary cortical neurons. However, the protective effects were abrogated under active-b-catenin-deficient conditions. Together, the data presented here showed that Pro, a weak opioid analgesic drug, attenuates OxyHb-induced mitochondria-dependent apoptosis in an active-b-catenin-c-Myc-dependent manner.

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Inhibition of leukotriene B4 synthesis protects against early brain injury possibly via reducing the neutrophil-generated inflammatory response and oxidative stress after subarachnoid hemorrhage in rats

Cited by 21 publications

References 52 publications

MiR-146a Ameliorates Hemoglobin-Induced Microglial Inflammatory Response via TLR4/IRAK1/TRAF6 Associated Pathways

MiR-146a Ameliorates Hemoglobin-Induced Microglial Inflammatory Response via TLR4/IRAK1/TRAF6 Associated Pathways

Antioxidant Melatonin: Potential Functions in Improving Cerebral Autoregulation After Subarachnoid Hemorrhage

Propoxyphene Mediates Oxyhemoglobin-Induced Injury in Rat Cortical Neurons Through Up-Regulation of Active-β-Catenin

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