Comparison of cardioprotective and anti-inflammatory effects of ischemia pre- and postconditioning in rats with myocardial ischemia–reperfusion injury

Xiong, Jie; Wang, Qiang; Xue, Fu‐Shan; Yuan, Yuan-Jing; Li, Shan; Liu, Jianhua; Liao, Xu; Zhang, Yanming

doi:10.1007/s00011-010-0303-4

Cited by 24 publications

(13 citation statements)

References 34 publications

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“…In the present study, we demonstrated by using double immuno-fluorescence staining that ischemic postconditioning protects neuronal apoptosis via suppression of neuronal proapoptotic proteins. Although we did not investigate the effect of ischemic postconditioning on the activation of glial NF-κB, other researchers reported that ischemic postconditioning could inhibit the production of toxic cytokines TNFα and IL-1β induced by ischemia [31]. We thus speculate that the transient ischemia-induced activation of glial NF-κB/p65 might be inhibited by ischemic postconditioning.…”

Section: Discussionmentioning

confidence: 77%

“…Yin et al showed that preconditioning with mTOR inhibitor rapamycin rescued brain damage via attenuating the production of NF-κB/p65 caused by subsequent ischemia/reperfusion[46]. Although ischemic postconditioning and preconditioning might share common pathways to induce intrinsic protective mechanism such as modulation of ASIC1a, notch signaling and neuroinflammation, [47], [48], [31], our result showed that the effect of ischemic postconditioning on activation of NF-κB/p65 is inhibitive, which is opposite to the inducing effect produced by ischemic preconditioning.…”

Section: Discussionmentioning

confidence: 99%

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Protection of Ischemic Postconditioning against Neuronal Apoptosis Induced by Transient Focal Ischemia Is Associated with Attenuation of NF-κB/p65 Activation

et al. 2014

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Background and PurposeAccumulating evidences have demonstrated that nuclear factor κB/p65 plays a protective role in the protection of ischemic preconditioning and detrimental role in lethal ischemia-induced programmed cell death including apoptosis and autophagic death. However, its role in the protection of ischemic postconditioning is still unclear.MethodsRat MCAO model was used to produce transient focal ischemia. The procedure of ischemic postconditioning consisted of three cycles of 30 seconds reperfusion/reocclusion of MCA. The volume of cerebral infarction was measured by TTC staining and neuronal apoptosis was detected by TUNEL staining. Western blotting was used to analyze the changes in protein levels of Caspase-3, NF-κB/p65, phosphor- NF-κB/p65, IκBα, phosphor- IκBα, Noxa, Bim and Bax between rats treated with and without ischemic postconditioning. Laser scanning confocal microscopy was used to examine the distribution of NF-κB/p65 and Noxa.ResultsIschemic postconditioning made transient focal ischemia-induced infarct volume decrease obviously from 38.6%±5.8% to 23.5%±4.3%, and apoptosis rate reduce significantly from 46.5%±6.2 to 29.6%±5.3% at reperfusion 24 h following 2 h focal cerebral ischemia. Western blotting analysis showed that ischemic postconditioning suppressed markedly the reduction of NF-κB/p65 in cytoplasm, but elevated its content in nucleus either at reperfusion 6 h or 24 h. Moreover, the decrease of IκBα and the increase of phosphorylated IκBα and phosphorylated NF-κB/p65 at indicated reperfusion time were reversed by ischemic postconditioning. Correspondingly, proapoptotic proteins Caspase-3, cleaved Caspase-3, Noxa, Bim and Bax were all mitigated significantly by ischemic postconditioning. Confocal microscopy revealed that ischemic postconditioning not only attenuated ischemia-induced translocation of NF-κB/p65 from neuronal cytoplasm to nucleus, but also inhibited the abnormal expression of proapoptotic protein Noxa within neurons.ConclusionsWe demonstrated in this study that the protection of ischemic postconditioning on neuronal apoptosis caused by transient focal ischemia is associated with attenuation of the activation of NF-κB/p65 in neurons.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Protection of Ischemic Postconditioning against Neuronal Apoptosis Induced by Transient Focal Ischemia Is Associated with Attenuation of NF-κB/p65 Activation

et al. 2014

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“…Neuroinflammation mediated by TLR2 or TLR4 was proved to play an active role in aggravating brain damage caused by ischemia/reperfusion. Under ischemic stimuli, TLR2 and TLR4 are both found to be expressed on neurons and glial cells such as microglia and astrocytes and would be activated when they are attached to their corresponding ligands such as heat-shock proteins (HSPs) and high mobility group box 1 (HMGB1) [9]. By contrast, inhibition of TLR2 or TLR4 pathway was reported to produce neuroprotection.…”

Section: Introductionmentioning

confidence: 99%

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Wang

Yang

et al. 2014

J Neuroinflammation

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Background and purposeIschemic postconditioning has been demonstrated to be a protective procedure to brain damage caused by transient focal ischemia/reperfusion. However, it is elusive whether the protection of postconditioning against brain damage and neuroinflammation is via regulating TLR2 and TLR4 pathways. In the present study, we examined the protection of ischemic postconditioning performed immediately prior to the recovery of cerebral blood supply on brain damage caused by various duration of ischemia and tested the hypothesis that its protection is via inhibition of neuroinflammation by modulating TLR2/TLR4 pathways.MethodsBrain damage in rats was induced by using the middle cerebral artery occlusion (MCAO) model. Ischemic postconditioning consisting of fivecycles of ten seconds of ischemia and reperfusion was performed immediately following theischemic episode Theduration of administration of ischemic postconditioning was examined by comparing its effects on infarction volume, cerebral edema and neurological function in 2, 3, 4, 4.5and 6 hour ischemia groups. The protective mechanism of ischemic postconditioning was investigated by comparing its effects on apoptosis, production of the neurotoxic cytokine IL-1β and the transcription and expression of TLR2, TLR4 and IRAK4 in the 2 and 4.5 hour ischemia groups.ResultsIschemic postconditioning significantly attenuated cerebral infarction, cerebral edema and neurological dysfunction in ischemia groups of up to 4 hours duration, but not in 4.5and 6 hour ischemia groups. It also inhibited apoptosis, production of IL-1β, abnormal transcription and expression of TLR2, TLR4 and IRAK4 in the 2 hour ischemia group, but not in the 4.5 hour ischemia group.ConclusionsIschemic postconditioning protected brain damage caused by 2, 3 and 4 hours of ischemia, but not by 4.5 and 6 hours of ischemia. The protection of ischemic postconditioning is associated with its inhibition of neuroinflammation via inhibition of TLR2 and TLR4 pathways.

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“…Michaelis et al (32) reported that glycyrrhizin may have anti-oxidative and anti-inflammatory effects in H5N1 influenza A virus-infected cells, through reducing the activation of JNK and p38. HMGB-1 is a highly conservative nucleoprotein that is released by necrotic or injured cells and secreted by mononuclear cells, and/or macrophages, which react with endogenous and exogenous non-inflammatory stimuli (33). HMGB-1 is secreted out of cells by non-classical and mediated secretory pathways, with HMGB-1 secretion occurring later than pro-inflammatory cytokines, including tumor necrosis factors (such as IL-1).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of glycyrrhizin on myocardial ischemia/reperfusion injury-induced oxidative stress, inducible nitric oxide synthase and inflammatory reactions through high-mobility group box 1 and mitogen-activated protein kinase expression

Cai

Wang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Glycyrrhizin, which is a type of perennial leguminous caudex, has been used in various Asian countries, including P.R. China, India and Japan, for thousands of years. The present study was designed to investigate the protective effect of glycyrrhizin on myocardial ischemia/reperfusion (I/R) injury through oxidative stress, inducible nitric oxide synthase (iNOS), and inflammatory reactions via high-mobility group box 1 (HMGB1) and mitogen-activated protein kinase (MAPK) expression. Sprague-Dawley rats were divided into five groups: Sham; myocardial I/R injury + non-treated; myocardial I/R injury + 2 mg/kg glycyrrhizin; myocardial I/R injury + 4 mg/kg glycyrrhizin; and myocardial I/R injury + 10 mg/kg glycyrrhizin. Pre-treatment with glycyrrhizin significantly reduced infarct size and inhibited creatine kinase, creatine kinase-MB, lactate dehydrogenase and cardiac troponin T activities in rats with myocardial I/R injury. Furthermore, glycyrrhizin treatment significantly suppressed oxidative stress, iNOS protein expression and inflammatory reactions in rats with myocardial I/R injury. Additionally, treatment with glycyrrhizin significantly decreased the release of HMGB1 from the cerebral cortex into the serum in rats with myocardial I/R injury. Notably, glycyrrhizin significantly suppressed p-ERK, p-p38 MAPK and p-c-Jun N-terminal kinase protein expressions, and promoted extracellular signal-regulated kinase protein expression in rats with myocardial I/R injury. Collectively, the present study indicates that the protective effect of glycyrrhizin may reduce myocardial I/R injury through oxidative stress, iNOS and inflammatory reactions, via HMGB1 and MAPK expression.

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Comparison of cardioprotective and anti-inflammatory effects of ischemia pre- and postconditioning in rats with myocardial ischemia–reperfusion injury

Abstract: In the rats with myocardial IRI in vivo, both IPC and IPOC can produce significant cardioprotective and anti-inflammatory effects. However, cardioprotective and anti-inflammatory effects provided by IPOC are weaker than with IPC.

Cited by 24 publications

References 34 publications

Protection of Ischemic Postconditioning against Neuronal Apoptosis Induced by Transient Focal Ischemia Is Associated with Attenuation of NF-κB/p65 Activation

Protection of Ischemic Postconditioning against Neuronal Apoptosis Induced by Transient Focal Ischemia Is Associated with Attenuation of NF-κB/p65 Activation

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Protective effect of glycyrrhizin on myocardial ischemia/reperfusion injury-induced oxidative stress, inducible nitric oxide synthase and inflammatory reactions through high-mobility group box 1 and mitogen-activated protein kinase expression

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