Kukoamine A Prevents Radiation-Induced Neuroinflammation and Preserves Hippocampal Neurogenesis in Rats by Inhibiting Activation of NF-κB and AP-1

Zhang, Yaqiong; Gao, Lingyue; Cheng, Zhihua; Niu, Yixuan; Meng, Wei

doi:10.1007/s12640-016-9679-4

Cited by 36 publications

(32 citation statements)

References 46 publications

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“…TNF-α is a main pro-inflammatory cytokine, and is mainly produced by activated microglia during the neuroinflammation. Growing evidence showed that the overproduction of TNF-α by microglia contributes to pathophysiological changes observed in various neurologic diseases and brain injury [3, 29]. In addition to inflammation caused by ischemia/hypoxia, we also found CoCl 2 treatment induced cell apoptosis (Fig 2).…”

Section: Discussionsupporting

confidence: 52%

Intracellular Ca2+ homeostasis and JAK1/STAT3 pathway are involved in the protective effect of propofol on BV2 microglia against hypoxia-induced inflammation and apoptosis

Lü

Ding

et al. 2017

PLoS ONE

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BackgroundPerioperative hypoxia may induce microglial inflammation and apoptosis, resulting in brain injury. The neuroprotective effect of propofol against hypoxia has been reported, but the underlying mechanisms are far from clear. In this study, we explored whether and how propofol could attenuate microglia BV2 cells from CoCl2-induced hypoxic injury.MethodsMouse microglia BV2 cells were pretreated with propofol, and then stimulated with CoCl2. TNF-α level in the culture medium was measured by ELISA kit. Cell apoptosis and intracellular calcium concentration were measured by flow cytometry analysis. The effect of propofol on CoCl2-modulated expression of Ca2+/Calmodulin (CaM)-dependent protein kinase II (CAMKIIα), phosphorylated CAMKIIα (pCAMKIIα), STAT3, pSTAT3Y705, pSTAT3S727, ERK1/2, pERK1/2, pNFκB(p65), pro-caspase3, cleaved caspase 3, JAK1, pJAK1, JAK2, pJAK2 were detected by Western blot.ResultsIn BV2 cell, CoCl2 treatment time-dependently increased TNF-α release and induced apoptosis, which were alleviated by propofol. CoCl2 (500μmol/L, 8h) treatment increased intracellular Ca2+ level, and caused the phosphorylation of CAMKIIα, ERK1/2 and NFκB (p65), as well as the activation of caspase 3. More importantly, these effects could be modulated by 25μmol/L propofol via maintaining intracellular Ca2+ homeostasis and via up-regulating the phosphorylation of JAK1 and STAT3 at Tyr705.ConclusionPropofol could protect BV2 microglia from hypoxia-induced inflammation and apoptosis. The potential mechanisms may involve the maintaining of intracellular Ca2+ homeostasis and the activation of JAK1/STAT3 pathway.

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Section: Discussionsupporting

confidence: 52%

Intracellular Ca2+ homeostasis and JAK1/STAT3 pathway are involved in the protective effect of propofol on BV2 microglia against hypoxia-induced inflammation and apoptosis

Lü

Ding

et al. 2017

PLoS ONE

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“…The IL-1β and TNF-α levels were measured using commercial ELISA kits as per the manufacturer’s instructions. 21 …”

Section: Methodsmentioning

confidence: 99%

Honokiol ameliorates radiation-induced brain injury via the activation of SIRT3

et al. 2020

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Objective Sirtuin 3 (SIRT3) plays a vital role in regulating oxidative stress in tissue injury. The aim of this study was to evaluate the radioprotective effects of honokiol (HKL) in a zebrafish model of radiation-induced brain injury and in HT22 cells. Methods The levels of reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) were evaluated in the zebrafish brain and HT22 cells. The expression levels of SIRT3 and cyclooxygenase-2 (COX-2) were measured using western blot assays and real-time polymerase chain reaction (RT-PCR). Results HKL treatment attenuated the levels of ROS, TNF-α, and IL-1β in both the in vivo and in vitro models of irradiation injury. Furthermore, HKL treatment increased the expression of SIRT3 and decreased the expression of COX-2. The radioprotective effects of HKL were achieved via SIRT3 activation. Conclusions HKL attenuated oxidative stress and pro-inflammatory responses in a SIRT3-dependent manner in radiation-induced brain injury.

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“…The results were recorded using Quantity One imaging software (Bio-Rad, Hercules, CA, USA), and relative intensities were calculated using Gel-Pro Analyzer software (Media Cybernetics, Bethesda, MD, USA). For some experiments, subcellular fractionation was performed using a Nuclear and Cytoplasmic Protein Extraction Kit (p0027, Beyotime Biotechnology, Shanghai, China) [ 36 , 37 ] and Tissue Mitochondria Isolation Kit (C3606, Beyotime Biotechnology) [ 38 , 39 ].…”

Section: Methodsmentioning

confidence: 99%

Ischemic Postconditioning Alleviates Cerebral Ischemia–Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats

Sun

Zhang

et al. 2018

Neurochem Res

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This study aimed to investigate whether ischemic postconditioning (IpostC) alleviates cerebral ischemia/reperfusion (I/R) injury involved in autophagy. Adult Sprague–Dawley rats were divided into five groups: sham (sham surgery), I/R (middle cerebral artery occlusion [MCAO] for 100 min, then reperfusion), IpostC (MCAO for 100 min, reperfusion for 10 min, MCAO for 10 min, then reperfusion), IpostC+3MA (3-methyladenine, an autophagy inhibitor, administered 30 min before first reperfusion), and IpostC+Veh (vehicle control for IpostC+3MA group). Infarct volume was measured using cresyl violet staining. Autophagy-related proteins were detected by western blot and immunohistochemistry. Autophagosomes, autophagolysosomes, and mitochondrial damage were identified by transmission electron microscopy. Cortical cell apoptosis was detected by the TUNEL assay. Neurologic function was assessed using the modified Neurologic Severity Score. IpostC improved neurological function and reduced infarct volume after I/R (P < 0.05). These effects of IpostC were inhibited by 3MA (P < 0.05). Autophagosome formation was increased in the I/R and IpostC+Veh groups (P < 0.05), but not in the IpostC+3MA group. The I/R group showed enhanced LC3-II/LC3-I ratio, p62, and Cathepsin B levels and decreased LAMP-2 level (all P < 0.05 vs. sham), indicating dysfunction of autophagic clearance. IpostC reduced p62 and Cathepsin B levels and increased the LC3-II/LC3-I ratio, and nuclear translocation of transcription factor EB (all P < 0.05); these effects of IpostC were reversed by 3MA, suggesting IpostC enhanced autophagic flux. Furthermore, IpostC attenuated I/R-induced mitochondrial translocation of Bax and mitochondrial cytochrome-c release (all P < 0.05); 3MA inhibited these effects of IpostC (P < 0.05). In conclusion, IpostC may alleviate cerebral I/R injury by activating autophagy during early reperfusion.Electronic supplementary materialThe online version of this article (10.1007/s11064-018-2599-3) contains supplementary material, which is available to authorized users.

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Kukoamine A Prevents Radiation-Induced Neuroinflammation and Preserves Hippocampal Neurogenesis in Rats by Inhibiting Activation of NF-κB and AP-1

Cited by 36 publications

References 46 publications

Intracellular Ca2+ homeostasis and JAK1/STAT3 pathway are involved in the protective effect of propofol on BV2 microglia against hypoxia-induced inflammation and apoptosis

Intracellular Ca2+ homeostasis and JAK1/STAT3 pathway are involved in the protective effect of propofol on BV2 microglia against hypoxia-induced inflammation and apoptosis

Honokiol ameliorates radiation-induced brain injury via the activation of SIRT3

Ischemic Postconditioning Alleviates Cerebral Ischemia–Reperfusion Injury Through Activating Autophagy During Early Reperfusion in Rats

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