The neuroprotective mechanism of brain ischemic preconditioning

Liu, Xiaoqian; Sheng, Rui; Qin, Zheng‐Hong

doi:10.1038/aps.2009.105

Cited by 133 publications

(103 citation statements)

References 90 publications

(102 reference statements)

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“…Therefore, induction of HSPs by the PGE1+Li mixture may play an important role in protecting neurons against ischemia-induced injury. Overexpression of HSPs protects neurons against apoptotic and necrotic cell death during cerebral ischemia [4,26] . Thus, the combined treatment enhanced the changes in the expression levels of pro-apoptotic and antiapoptotic proteins.…”

Section: Discussionmentioning

confidence: 99%

“…HSPs may exert neuroprotective effects by antagonizing apoptotic and necrotic cell death during cerebral ischemia [3] . Induction of HSPs also plays a role in the preconditioning-induced resistance of neurons to ischemic insults [4,5] . HSPs such as HSP70, glucose-regulated protein 78 (GRP78) and HSP60 are important regulators of cellular survival and may be used as potential therapeutic targets for treating ischemic neuronal injury [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

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Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia

et al. 2011

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Aim: To examine the effects of a mixed formulation composed of prostaglandin E1 and lithium (PGE1+Li mixture) on brain damage after cerebral ischemia. The effects of the mixture on protein expression of heat shock proteins (HSPs), p53, and Bcl-2 were also determined. Methods: Brain ischemia was induced with a permanent middle cerebral artery occlusion (pMCAO) in rats. Rats were treated with a single intravenous administration of PGE1, lithium or a PGE1+Li mixture immediately after the ischemic insult. The infarct volume and motor behavior deficits were analyzed 24 h after the ischemic insult. The protein levels of HSP70, glucose-regulated protein 78 (GRP78), HSP60, Bcl-2, and p53 in the striatum of the ipsilateral hemisphere were examined using immunoblotting. Results: The mixture (PGE1 22.6 nmol/kg+Li 0.5 mmol/kg) reduced infarct volume and neurological deficits induced by focal cerebral ischemia. Moreover, the mixture had a greater neuroprotective effect against cerebral ischemia compared with PGE1 or lithium alone. The mixture was effective even if it was administered 3 h after ischemia. PGE1+Li also significantly upregulated cytoprotective HSP70, GRP78, HSP60, and Bcl-2 protein levels, while decreasing p53 expression. Conclusion: These results demonstrated a PGE1+Li mixture with a therapeutic window of up to 3 h for clinical treatment of cerebral ischemia. The PGE1+Li mixture potentially exerts a protective effect after stroke through the induction of HSPs and Bcl-2 proteins.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia

et al. 2011

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“…Indeed, lacking the A 1 receptor exhibited decreased hypoxic neuroprotection in mice (Johansson et al 2001 ) . Thus, Ado may be involved in ischemic preconditioning, an endogenous neuroprotective mechanism (Liu et al 2009 ) . Consequently, drugs that act on adenosine receptors, adenosine metabolizing enzymes, and nucleoside transporters (Table 29.2 , Fig.…”

Section: Strokementioning

confidence: 99%

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

Kovács

Dobolyi

2012

Adenosine

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Nucleosides have a wide range of physiological and pathophysiological roles in the human brain as modulators of a variety of neural functions. For example, adenosine, inosine, guanosine, and uridine participate in the mechanisms underlying memory, cognition, sleep, pain, depression, schizophrenia, epilepsy, Alzheimer's disease, Huntington's disease, and Parkinson's disease. Consequently, increasing attention is now being given to the speci fi c role of nucleosides in physiological and pathological processes in the human brain. Different elements of nucleoside system, including nucleoside concentrations, metabolic enzyme activity, and expression of nucleoside transporters and receptors, may be changed under normal and pathological conditions. The alterations suggest that interlinked elements of the nucleoside system are functioning in a tightly concerted manner.Nucleoside levels, activity of nucleoside metabolic enzymes, and expression of nucleoside transporters and receptors are unevenly distributed in the brain, suggesting that nucleosides have different roles in functionally distinct human brain areas. The aim of this chapter is to summarize our present knowledge of the anatomical distribution of nucleoside system in the human brain, placing emphasis on potential therapeutic pharmacological strategies.

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“…This phenomenon is known as ischemic preconditioning (IPC). Studying IPC may provide insight into endogenous protective mechanisms that could be exploited therapeutically [1][2][3][4] . The endoplasmic reticulum (ER) is an organelle in which secretory or membrane proteins are synthesized.…”

Section: Introductionmentioning

confidence: 99%

The endoplasmic reticulum stress inhibitor salubrinal inhibits the activation of autophagy and neuroprotection induced by brain ischemic preconditioning

et al. 2013

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Aim: To investigate whether endoplasmic reticulum (ER) stress participates in the neuroprotective effects of ischemic preconditioning (IPC)-induced neuroprotection and autophagy activation in rat brains. Methods: The right middle cerebral artery in SD rats was occluded for 10 min to induce focal cerebral IPC, and was occluded permanently 24 h later to induce permanent focal ischemia (PFI). ER stress inhibitor salubrinal (SAL) was injected via intracerebral ventricle infusion 10 min before the onset of IPC. Infarct volume and motor behavior deficits were examined after the ischemic insult. The protein levels of LC3, p62, HSP70, glucose-regulated protein 78 (GRP 78), p-eIF2α and caspase-12 in the ipsilateral cortex were analyzed using immunoblotting. LC3 expression pattern in the sections of ipsilateral cortex was observed with immunofluorescence. Results: Pretreatment with SAL (150 pmol) abolished the neuroprotective effects of IPC, as evidenced by the significant increases in mortality, infarct volume and motor deficits after PFI. At the molecular levels, pretreatment with SAL (150 pmol) significantly increased p-eIF2α level, and decreased GRP78 level after PFI, suggesting that SAL effectively inhibited ER stress in the cortex. Furthermore, the pretreatment with SAL blocked the IPC-induced upregulation of LC3-II and downregulation of p62 in the cortex, thus inhibiting the activation of autophagy. Moreover,SAL blocked the upregulation of HSP70, but significantly increased the cleaved caspase-12 level, thus promoting ER stress-dependent apoptotic signaling in the cortex. Conclusion: ER stress-induced autophagy might contribute to the neuroprotective effect of brain ischemic preconditioning.

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The neuroprotective mechanism of brain ischemic preconditioning

Cited by 133 publications

References 90 publications

Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia

Combined prostaglandin E1 and lithium exert potent neuroprotection in a rat model of cerebral ischemia

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

The endoplasmic reticulum stress inhibitor salubrinal inhibits the activation of autophagy and neuroprotection induced by brain ischemic preconditioning

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