Cyclophilin A/Cluster of Differentiation 147 Interactions Participate in Early Brain Injury After Subarachnoid Hemorrhage in Rats

Dang, Baoqi; Li, Haiying; Xu, Xiang; Shen, Haitao; Wang, Yan; Gao, Anju; He, Weichun; Wang, Zhong; Chen, Gang

doi:10.1097/ccm.0000000000001146

Cited by 42 publications

(34 citation statements)

References 48 publications

(67 reference statements)

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“…The transfection of Nrf2 siRNA for rat brains in vivo were conducted according to the method described formerly [17, 31, 32]. Briefly, the rats were placed under anesthesia, then a cranial burr hole (1 mm in diameter) was drilled, following a 25-μl microsyringe with a needle tip (Shanghai high pigeon industry & trade co., LTD, Shanghai, China) was inserted stereotaxically into the right lateral ventricle.…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, the rats were placed under anesthesia, then a cranial burr hole (1 mm in diameter) was drilled, following a 25-μl microsyringe with a needle tip (Shanghai high pigeon industry & trade co., LTD, Shanghai, China) was inserted stereotaxically into the right lateral ventricle. The stereotaxic coordinates were 1.5 mm posterior, 1.0 mm lateral, and 3.2 mm below the horizontal plane of the bregma [32]. Nrf2 siRNA (sc-156128, Santa Cruz biotechnology, USA) and control scramble siRNA (sc-37007, Santa Cruz Biotechnology, USA) were applied with in vivo transfection reagent (Entranster TM -in vivo, 18668-11-1, Engreen Biosystem Co, Ltd., Beijing, China) at 24 h before modeling by intracerebroventricular injection [31, 32].…”

Section: Methodsmentioning

confidence: 99%

“…The stereotaxic coordinates were 1.5 mm posterior, 1.0 mm lateral, and 3.2 mm below the horizontal plane of the bregma [32]. Nrf2 siRNA (sc-156128, Santa Cruz biotechnology, USA) and control scramble siRNA (sc-37007, Santa Cruz Biotechnology, USA) were applied with in vivo transfection reagent (Entranster TM -in vivo, 18668-11-1, Engreen Biosystem Co, Ltd., Beijing, China) at 24 h before modeling by intracerebroventricular injection [31, 32]. The microsyringe was left in place for an additional 10 min after administration and then slowly withdrawn.…”

Section: Methodsmentioning

confidence: 99%

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Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

Zeng

Chen

Ding

et al. 2017

J Neuroinflammation

280

214

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BackgroundIntracerebral hemorrhage (ICH) induces potently oxidative stress responses and inflammatory processes. Isoliquiritigenin (ILG) is a flavonoid with a chalcone structure and can activate nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant system, negatively regulate nuclear factor-κB (NF-κB) and nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathways, but its role and potential molecular mechanisms in the pathology following ICH remain unclear. The present study aimed to explore the effects of ILG after ICH and underlying mechanisms.MethodsICH model was induced by collagenase IV (0.2 U in 1 μl sterile normal saline) in male Sprague-Dawley rats weighing 280–320 g. Different doses of ILG (10, 20, or 40 mg/kg) was administrated intraperitoneally at 30 min, 12 h, 24 h, and 48 h after modeling, respectively. Rats were intracerebroventricularly administrated with control scramble small interfering RNA (siRNA) or Nrf2 siRNA at 24 h before ICH induction, and after 24 h, ICH model was established with or without ILG (20 mg/kg) treatment. All rats were dedicated at 24 or 72 h after ICH. Neurological deficits, histological damages, brain water content (BWC), blood-brain barrier (BBB) disruption, and neuronal degeneration were evaluated; quantitative real-time RT-PCR (qRT-PCR), immunohistochemistry/immunofluorescence, western blot, and enzyme-linked immunosorbent assay (ELISA) were carried out; catalase, superoxide dismutase activities and reactive oxygen species (ROS), and glutathione/oxidized glutathione contents were measured.ResultsILG (20 and 40 mg/kg) markedly alleviated neurological deficits, histological damages, BBB disruption, brain edema, and neuronal degeneration, but there was no significant difference between two dosages. ILG (20 mg/kg) significantly suppressed the NF-κB and NLRP3 inflammasome pathways and activated Nrf2-mediated antioxidant system. Gene silencing of Nrf2 aggravated the neurological deficits, brain edema, and neuronal degeneration and increased the protein levels of NF-κB p65, NLRP3 inflammasome components, and IL-1β. ILG delivery significantly attenuated the effects of Nrf2 siRNA interference mentioned above.ConclusionsIntraperitoneal administration of ILG after ICH reduced early brain impairments and neurological deficits, and the mechanisms were involved in the regulation of ROS and/or NF-κB on the activation of NLRP3 inflammasome pathway by the triggering of Nrf2 activity and Nrf2-induced antioxidant system. In addition, our experimental results may make ILG a potential candidate for a novel therapeutical strategy for ICH.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0895-5) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

Zeng

Chen

Ding

et al. 2017

J Neuroinflammation

280

214

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“…In part II, fifty‐four male rats were divided into three groups, sham group, control siRNA group (TBI group), and Lats1 siRNA group (18 rats each; n = 18), according to the randomized grouping method. First, we used stereotaxic instrument to performed intraventricular injection of siRNA vehicle and Lats1 siRNA (20 μL, 500 pmol/20 μL) . At 24 hours after intracerebroventricular injection, the rats in control siRNA group (TBI group) and Lats1 siRNA group were performed brain trauma.…”

Section: Methodsmentioning

confidence: 99%

“…First, we used stereotaxic instrument to performed intraventricular injection of siRNA vehicle and Lats1 siRNA (20 μL, 500 pmol/20 μL). 17 At 24 hours after intracerebroventricular injection, the rats in control siRNA group (TBI group) and Lats1 siRNA group were performed brain trauma. Meanwhile, the sham group was treated with a sham wound.…”

Section: Part IImentioning

confidence: 99%

Inhibition of Lats1/p‐YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of traumatic brain injury

et al. 2018

CNS Neurosci Ther

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Role of Exosomes Derived from miR-133b Modified MSCs in an Experimental Rat Model of Intracerebral Hemorrhage

Shen

Yao

et al. 2018

J Mol Neurosci

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Intracerebral hemorrhage (ICH) has poor outcomes due to high mortality and morbidity, but until now, the effective treatments remain limited. MicroRNAs (miRNAs) are vital regulators of gene expression and demonstrated to be linked to the pathogenesis of various central nervous system (CNS) diseases. Exosomes are considered as cell-to-cell communication vectors and secreted largely by mesenchymal stromal cells (MSCs). The present study investigated the role of miR-133b delivered by exosomes secreted from MSCs to brain tissues in rats after ICH. An autologous arterial blood ICH model in adult male Sprague-Dawley (SD) rats was used in this study. At 72 h after transfection with miR-133b mimics in MSCs, miR-133b-modified MSC-derived exosomes were collected from medium of MSCs and then injected to rats via tail vein. The levels of miR-133b in secreted exosomes and brain tissues of rats in various groups and the levels of RhoA, phosphorylations of extracellular signal regulating kinase (ERK1/2), and cAMP response element-binding protein (CREB) were detected by real-time PCR and western blot analysis, respectively. The effects of miR-133b on neuronal apoptosis and degeneration were respectively evaluated by TUNEL and fluoro-jade B staining. The miR-133b levels were reduced in brain tissues of rats at 24 h and peaked at 72 h after ICH. At 24 h after miR-133b-modified exosome administration, the level of miR-133b was significantly increased, while the apoptotic and neurodegenerative neurons were obviously reduced in brain tissues after ICH. The results of western blot analysis showed that miR-133b modified exosomes treatment remarkably suppressed RhoA expression and activated ERK1/2/CREB in brain tissues after ICH. Collectively, our investigation suggested that exosomes derived from miR-133b modified MSCs exhibited neuroprotective role for anti-apoptotic effect of miR-133b mediating RhoA and ERK1/2/CREB in rats after ICH.

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Cyclophilin A/Cluster of Differentiation 147 Interactions Participate in Early Brain Injury After Subarachnoid Hemorrhage in Rats

Cited by 42 publications

References 48 publications

Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

Inhibition of Lats1/p‐YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of traumatic brain injury

Role of Exosomes Derived from miR-133b Modified MSCs in an Experimental Rat Model of Intracerebral Hemorrhage

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