Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-κB pathway

Lan, Lan; Tao, Jing; Chen, Azhen; Xie, Guanli; Hua, Jia; Lin, Jiumao; Peng, Jun; Chen, Lidian

doi:10.3892/ijmm.2012.1184

Cited by 116 publications

(85 citation statements)

References 29 publications

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“…EA was a proven, effective therapy for ameliorating the injured learning and memory induced by the AMIR event (Lan et al, 2013), but the underlying mechanisms remained uncertain. In the present study, we proved that EA treatment reduced the side effects of AMIR, which included improving survival rate, alleviating hippocampal histopathological damage, inhibiting the neuronic peroxidatic reaction within the hippocampal tissue and attenuating the inflammation in the central and peripheral nervous systems.…”

Section: Discussionmentioning

confidence: 99%

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia–reperfusion

Yuan

Zhang

et al. 2014

Brain Research

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Section: Discussionmentioning

confidence: 99%

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia–reperfusion

Yuan

Zhang

et al. 2014

Brain Research

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“…Cerebral infarction volume was determined using 2, 3,5 triphenyltetrazolium chloride (TTC) staining of brains after MCAO as previously descripted [29]. The dissected brain splices (2 mm thick) were incubated with a 2% TTC solution at 37°C for 20 min.…”

Section: Methodsmentioning

confidence: 99%

Down-Regulation of Lncrna MALAT1 Attenuates Neuronal Cell Death Through Suppressing Beclin1-Dependent Autophagy by Regulating Mir-30a in Cerebral Ischemic Stroke

Guo¹,

Ma²,

Yan³

et al. 2017

Cell Physiol Biochem

151

100

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Background/Aims: LncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported to be highly expressed in an in vitro mimic of ischemic stroke conditions. However, the exact biological role of MALAT1 and its underlying mechanism in ischemic stroke remain to be elucidated. Methods: The roles of MALAT1 and miR-30a on cell death and infarct volume and autophagy were evaluated in experimental ischemic stroke. The relationships between miR-30a and MALAT1, Beclin1 were confirmed by luciferase reporter assay. The autophagy inhibitor 3-methyadenine (3-MA) was used to examine the impact of autophagy on ischemic injury. Results: We found that MALAT1, along with the levels of conversion from autophagy-related protein microtubule-associated protein light chain 3-I (LC3-I) to LC3-phosphatidylethanolamine conjugate (LC3-II), as well as Beclin1 were up-regulated and miR-30a was down-regulated in cerebral cortex neurons after oxygen-glucose deprivation (OGD) and mouse brain cortex after middle cerebral artery occlusion-reperfusion (MCAO). Down-regulation of MALAT1 suppressed ischemic injury and autophagy in vitro and in vivo. Furthermore, MALAT1 may serve as a molecular sponge for miR-30a and negatively regulate its expression. In addition, MALAT1 overturned the inhibitory effect of miR-30a on ischemic injury and autophagy in vitro and in vivo, which might be involved in the derepression of Beclin1, a direct target of miR-30a. Mechanistic analyses further revealed that autophagy inhibitor 3-methyadenine (3-MA) markedly suppressed OGD-induced neuronal cell death and MCAO-induced ischemic brain infarction. Conclusion: Taken together, our study first revealed that down-regulation of MALAT1 attenuated neuronal cell death through suppressing Beclin1-dependent autophagy by regulating miR-30a expression in cerebral ischemic stroke. Besides, our study demonstrated a novel lncRNA-miRNA-mRNA regulatory network that is MALAT1-miR-30a-Beclin1 in ischemic stroke, contributing to a better understanding the pathogenesis and progression of ischemic stroke.

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“…Nuclear factor-κB (NF-κB) is a transcription factor that has crucial roles in inflammation, immunity, cell proliferation and apoptosis (4)(5)(6). Activation of NF-κB is controlled by the inhibitor of κB (I-κB), which retains NF-κB in the cytoplasm (7).…”

Section: Introductionmentioning

confidence: 99%

Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

Zhang

2014

Molecular Medicine Reports

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Abstract. Intermittent hypoxia/reoxygenation (IHR) induces proinflammatory cytokines, contributing to the pathogenic process of atherosclerosis associated with obstructive sleep apnea (OSA). Two transcription factors, nuclear factor-κB (NF-κB) and hypoxia-inducible factor-1 (HIF-1), have been indicated to mediate proinflammatory cytokines during IHR. The anti-inflammatory effects of propofol have attracted increasing attention in regard to the treament of multiple diseases associated with inflammation. The present study examined whether propofol inhibits NF-κB and HIF-1 activity in vascular endothelial cells during IHR. EA.hy926 endothelial cells were exposed to IHR for 64 cycles with or without propofol treatment. Gene knockdown by transfection of siRNA against p38 mitogen-activated protein kinase (MAPK) was also used to investigate the molecular mechanisms. Compared with the control group, IHR exposure significantly induced the activation of NF-κB and HIF-1, enhanced the mRNA expression of proinflammatory cytokines and increased the activation of p38 MAPK. Propofol dose-dependently inhibited the IHR-induced activation of NF-κB, but did not change the activation of HIF-1, which was accompanied by decreased levels of proinflammatory cytokines. In addition, IHR-induced p38 MAPK activity was attenuated by propofol in a similar manner to the reduction in NF-κB activity. Furthermore, knockdown of p38 MAPK with siRNA significantly reduced the IHR-induced activation of NF-κB, while not affecting HIF-1. These data demonstrate that propofol selectively attenuates the IHR-induced activation of NF-κB, but not HIF-1, in vascular endothelial cells, and these beneficial effects are likely to be based on the inhibition of the p38 MAPK signaling pathway. Propofol may have the potential to prevent atherosclerosis in patients with OSA by inhibiting NF-κB-mediated inflammation in the vascular endothelium.

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Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-κB pathway

Cited by 116 publications

References 29 publications

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia–reperfusion

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia–reperfusion

Down-Regulation of Lncrna MALAT1 Attenuates Neuronal Cell Death Through Suppressing Beclin1-Dependent Autophagy by Regulating Mir-30a in Cerebral Ischemic Stroke

Propofol selectively inhibits nuclear factor-κB activity by suppressing p38 mitogen-activated protein kinase signaling in human EA.hy926 endothelial cells during intermittent hypoxia/reoxygenation

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