Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Ma, Di; Feng, Lei; Deng, Fang; Feng, Jiachun

doi:10.1155/2017/6891645

Cited by 15 publications

(13 citation statements)

References 79 publications

(98 reference statements)

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“…Th1 cells play an stimulating inflammatory response role following stroke, with secreting pro-inflammatory cytokines including interferon-γ (IFN-γ), and tumor necrosis factor (TNF)-β, whereas Th2 cells have an inhibitory effect on inflammation response via producing anti-inflammatory cytokines like interleukin (IL)- 4, IL-5, IL-10, and IL-13 [ 25 ]. The information described above resolves the controversial issue of whether a lower lymphocyte count is independently associated with poor outcome at 3 months [ 7 , 26 ]. Following stroke, patients may have lymphopenia or a reduction in absolute lymphocyte count, a phenomenon of immunodepression, which might due to activation of the hypothalamic-pituitary-adrenal system, sympathetic nervous system, and parasympathetic nervous system, with the secretion and release of cortisol, catecholamines, and acetylcholine, contributing to lymphocyte apoptosis [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Decreased Lymphocyte-to-Monocyte Ratio Predicts Poor Prognosis of Acute Ischemic Stroke Treated with Thrombolysis

et al. 2017

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BackgroundOur previous study found that lower lymphocyte-to-monocyte ratio (LMR) is an independent risk factor of clinical outcome of acute ischemic stroke (AIS). However, whether lower LMR is independently associated with adverse prognosis of AIS treated with thrombolysis has not been determined. In this study, we explored the relationship between LMR and prognosis of AIS treated with thrombolysis.Material/MethodsWe retrospectively enrolled 108 patients treated with thrombolysis. LMR was calculated according to lymphocyte count and monocyte count on admission. Patients were classified into 3 groups according to LMR values on admission (group 1 LMR >4.34, group 2 LMR 2.79 to 4.34, group 3 LMR <2.79). Neurologic impairment was estimated by use of the National Institute of Health Stroke Scale. Clinical prognosis at 3 months was assessed by modified Rankin Scale. The relationship between LMR and neurologic impairment was analyzed by Spearman rank correlation. Receiver operating characteristic curve (ROC) was used to evaluate the ability of LMR to predict outcome.ResultsPatients in group 3 had lower lymphocyte counts and LMR values and higher monocyte counts (P<0.001). LMR value was negatively correlated with the degree of neurologic impairment (r=−0.372, P<0.001). The ROC suggested a moderate sensitivity (71.6%) and specificity (80.5%) of LMR for predicting prognosis with an optimal cut-off point at 3.48. Higher LMR value was an independent protective factor against adverse prognosis (odds ratio 0.683, 95% confidence interval 0.490−0.952, P=0.024).ConclusionsA lower LMR value is an independent predictor of poor prognosis of AIS treated with thrombolytic therapy.

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Section: Discussionmentioning

confidence: 99%

Decreased Lymphocyte-to-Monocyte Ratio Predicts Poor Prognosis of Acute Ischemic Stroke Treated with Thrombolysis

et al. 2017

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“…Recently, studies have reported that markedly increased autophagy following the upregulation of LC3 and downregulation of P62 in the peri-infarct areas following ischemia may reduce the infarct size, which was also validated in the vascular endotheliocytes and neurons in the AMCAO group. In comparison with the PMCAO control group, the number of vascular endothelial cells and neurons was higher after ATV pretreatment, and the ratio of P62-labeled cells/DAPI, P62 protein levels, the ratio of LC3-labeled neurons and LC3II/LC3I were decreased ( Gao et al, 2012 ; Ma et al, 2017 ). Consistent with this phenomenon, 3MA pretreatment in the 3MAMCAO rats led to the stimulation of apoptosis and enlargement of the infarct, which were verified by the following results.…”

Section: Discussionmentioning

confidence: 80%

“…In addition to PERK, the other two ER membrane-associated proteins that activate the UPR were ATF6 ( Figure 6D ) and IRE1, and the latter promotes the phosphorylation of JNK, P38, and NF-κB kinase ( Figure 6B ). However, pretreatment with ATV disturbed the activation of chaperones such as Grp78/Bip dissociation from IRE1-α, PERK, and ATF6 during acute ER stress ( Yin et al, 2017 ), as well as calnexin, Nrf2 and Ero1-Lα, which participate in oxidative and Ca 2+ -related stress to regulate ER stress ( Giorgi et al, 2015 ) ( Figure 6C ), and downregulated the downstream activation of JNK, P38 and NF-κB kinase ( Figure 6B ) to inhibit the subsequent apoptosis ( Ma et al, 2017 ). Furthermore, there was no significance in the change in Ero1-Lα between the vehicle PMCAO and AMCAO groups ( Figure 6C ).…”

Section: Resultsmentioning

confidence: 99%

“…The autophagy processes in focal ischemia were disturbed by 3MA through the downregulation of LC3II and the upregulation of P62. Next, minimizing damage surrounding the ischemic areas requires the amelioration/prevention of cell apoptosis, which is the current vital therapeutic target in the treatment of acute ischemic stroke ( Ma et al, 2017 ). In the current study, the hypoxia-related protein HIF1α and the apoptotic protein cleaved-caspase 3 were attenuated, and the anti-apoptotic protein Bcl-2 was activated by ATV compared to that in the PMCAO group.…”

Section: Discussionmentioning

confidence: 99%

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HMG-CoA Reductase Inhibitors Relieve Endoplasmic Reticulum Stress by Autophagy Inhibition in Rats With Permanent Brain Ischemia

Zhang

Yang

et al. 2018

Front. Neurosci.

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Exploring and expanding the indications of common clinical drugs, such as statins, is important to improve the prognosis of patients with permanent cerebral infarction. It has been suggested that reversing the defects in cellular autophagy and ER stress with statin therapy may be a potential treatment option for reducing ischemic damage. Male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (PMCAO) by electrocoagulation surgery. Atorvastatin (ATV, 10 mg/kg/day) or vehicle was administered intraperitoneally. Rats were divided into the vehicle-treated (SHAM), ATV pretreatment for MCAO (AMCAO), and 3-methyladenine (3MA) combined with ATV pretreatment (3MAMCAO) groups. Magnetic resonance imaging, as well as immunohistochemical and Western blot assessments, were performed 24 h after MCAO. Each ATV-treated group demonstrated significant reductions in infarct volume compared with that in the vehicle-treated group at 24 h after MCAO, which was associated with autophagy reduction and ER stress attenuation in neurons and neovascularization. Next, Western blotting was used to detect the levels of the autophagy-related proteins LC3B and P62 and of ER stress pathway proteins. However, 3MA significantly partially inhibited the ER stress pathway via limiting the autophagic flux in the AMCAO group. In conclusion, our results imply that the neuroprotective function of ATV depends on autophagic activity to diminish ER stress-related cell apoptosis in rats with PMCAO and suggest that compounds that inhibit autophagic activity might reduce the neuroprotective effect of ATV after brain ischemia.

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“…Following a period of cerebral ischemia, ischemic postconditioning (IPostC), by applying a transient blood reperfusion/reocclusion series at the cerebral blood vessels, stimulates a variety of endogenous neuroprotective mechanisms and acts to reduce the effects of ischemia/reperfusion (I/R) injury [ 1 ]. However, clinical application of IPostC is limited due to the risk of additional ischemia to the brain.…”

Section: Introductionmentioning

confidence: 99%

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate

You

Feng

Xin

et al. 2018

BioMed Research International

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Following cerebral ischemia/reperfusion (I/R) injury, a series of pathophysiological processes are stimulated in both the central nervous system (CNS) and the periphery, including, but not limited to, the peripheral immune and endocrine systems and underregulation of the neuroendocrine-immune network. Glutamate (Glu) is an important excitatory neurotransmitter in the CNS; its excitotoxicity following cerebral ischemia has been a focus of study for several decades. In addition, as a novel immunoregulator, Glu also regulates immune activity in both the CNS and periphery and may connect the CNS and periphery through regulation of the neuroendocrine-immune network. Ischemic postconditioning (IPostC) is powerful and activates various endogenous neuroprotective mechanisms following cerebral I/R, but only a few studies have focused on the mechanisms associated with Glu to date. Given that Glu plays an important and complex pathophysiological role, the understanding of Glu-related mechanisms of IPostC is an interesting area of research, which we review here.

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Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Cited by 15 publications

References 79 publications

Decreased Lymphocyte-to-Monocyte Ratio Predicts Poor Prognosis of Acute Ischemic Stroke Treated with Thrombolysis

Decreased Lymphocyte-to-Monocyte Ratio Predicts Poor Prognosis of Acute Ischemic Stroke Treated with Thrombolysis

HMG-CoA Reductase Inhibitors Relieve Endoplasmic Reticulum Stress by Autophagy Inhibition in Rats With Permanent Brain Ischemia

Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate

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