Post-conditioning with gradually increased reperfusion provides better cardioprotection in rats

Zhang, Guoming; Wang, Yu; Li, Tian-de; Li, Xiaoyan; Shao-ping, SU; Sun, Yuhao; Li, Xiuhua

doi:10.5847/wjem.j.issn.1920-8642.2014.02.009

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…The expression of JNK and p38 was detected as described by Zhang et al [9] with Western blotting analysis. In brief, left ventricular myocardium was homogenized in ice-cold lysis buffer.…”

Section: Detection Of the Jnk And P38 Expressionmentioning

confidence: 99%

Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways

Chen

Zhang²,

Liu³

et al. 2016

Cell Physiol Biochem

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Background: The purpose of this study was to determine whether c-jun NH₂ amino-terminal kinases (JNK) and p38 mitogen-activated protein kinases (MAPK) were involved in morphine postconditioning (MpostC). Methods: The isolated rat hearts were randomly assigned into one of the following groups. Hearts in the time control (TC) group were constantly perfused for 105min. Hearts in the ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion. MpostC was induced by 10 min of morphine administration at the onset of reperfusion. Anisomycin (an activator of JNK/p38 kinases) was administered with or without morphine during the first 10 min of reperfusion following the 45 min of ischemia. Mitochondria and cytosolic proteins were prepared to detect mitochondrial permeability transition (MPT) and cytochrome C (Cyt-c) respectively. Results: MpostC markedly reduced infarct size (IS/AAR), CK-MB release, and improved cardiac function recovery. However, these protective effects were partly abolished in the presence of anisomycin. I/R significantly increased the phosphorylation of JNK and p38 kinases, mitochondrial permeability transition (MPT) opening and Cyt-c release, while these effects were partly abolished by MpostC. The inhibitory effects of MpostC on the phosphorylation of JNK/p38 kinases, MPT opening and Cyt-c release were totally reversed by Anisocycin, which, used individually, did not show any influence on perfusion injury. Conclusions: These findings suggest that MpostC protects isolated rat hearts against reperfusion injury via inhibiting JNK/p38 MAPKs and mitochondrial permeability transition pores signaling pathways.

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“…The expression of JNK and p38 was detected as described by Zhang et al [9] with Western blotting analysis. In brief, left ventricular myocardium was homogenized in ice-cold lysis buffer.…”

Section: Detection Of the Jnk And P38 Expressionmentioning

confidence: 99%

Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways

Chen

Zhang²,

Liu³

et al. 2016

Cell Physiol Biochem

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“…Recent developments in cardiac physiology have indicated that PostC significantly reduces infarct size and inhibits inflammation and apoptosis [17][18][19][20][21]. Zhao [22] at first documented that PostC reduced infarct size in cerebral I/R injury.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, the protective effect of RPostC against focal cerebral ischemia in rats was also verified [16]. However, its potential protective mechanisms have not been established.Recent developments in cardiac physiology have indicated that PostC significantly reduces infarct size and inhibits inflammation and apoptosis [17][18][19][20][21]. Zhao [22] at first documented that PostC reduced infarct size in cerebral I/R injury.…”

mentioning

confidence: 99%

Effects of Limb Remote Postconditioning on Apoptosis and Long-Term Neurological Outcomes of Focal Cerebral Ischemia/Reperfusion Injury in Rats

Li¹,

Jiang²

2015

J Diabetes Metab

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Background and Purpose: Remote ischemic postconditioning (RPostC) is an emerging concept for cerebral infarction protection, and it has better application prospects in clinical practice. However, little is known about the neuroprotection mechanisms of RPostC in cerebral ischemia/reperfusion (I/R) injury. In the present study, we investigated the effects of RPostC on neural cells apoptosis and long-term neurological outcomes in focal cerebral I/R injury in the rat middle cerebral artery occlusion model. Methods:Focal cerebral ischemia was induced by middle cerebral artery occlusion using the intraluminal filament technique in male rats. RPostC was generated by 3 cycles of femoral artery 10-minute occlusion/reperfusion on the right limb at the onset of middle cerebral artery reperfusion. Adult male wistar rats were treated with remote post conditioning after 90 minutes of occlusion (beginning of reperfusion). Infarct volumes were assessed at 24h and 21d of stroke onset. Neurological scores were assessed at 24h and 3d,5d, 7d,10d, 14, 21d after the onset of middle cerebral artery reperfusion. Apoptosis-related molecules were studied at 24h of stroke onset by Western blotting.Results: RPostC treatment up-regulated Bcl-2 and heat-shock protein 70 (HSP70) expression and downregulated Bax expression. RPostC treatment also reduced infarct volumes at 24h and 21d, meanwhile, it also improved the neurologic scores and the long-term neurological outcomes compared with the I/R-only group. Conclusion:These findings indicate that RPostC inhibits focal cerebral I/R injury and improves the neurological outcomes. This neuroprotective effect is likely achieved by anti-apoptotic mechanisms. Effects of Limb IntroductionBrain ischemia is becoming a leading cause of morbidity and mortality world-wide [1]. Its major pathophysiological manifestation is an acute brain ischemia-reperfusion injury [2]. Despite extensive researchs on reperfusion injury treatment in the past several decades, few neuroprotectants have been successfully from basic research into clinical application. A variety of clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing [3][4][5]. Therefore, innovative treatment strategies for protecting brain against the detrimental effects of this form of injury are required in order to improve clinical outcomes in patients with brain ischemic injury. Researchers are now interested in the brain's endogenous strategies for neuroprotection [6,7]. Harnessing the endogenous protection elicited by the brain's ability to "condition" itself has recently emerged as a powerful new strategy for limiting brain injury [8,9].Ischemic postconditioning (PostC), which is defined as rapid intermittent interruptions of blood flow in the early phase of reperfusion and mechanically alters the hydrodynamics of reperfusion, has been verified to protect tissues from I/R injury [10]. The clinical applicability of PostC is limited because PostC can interrupt intermittent reperfusion of vital organs and re...

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Toward the Question of Ischemic Myocardial Dysfunction

et al. 2014

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Post-conditioning with gradually increased reperfusion provides better cardioprotection in rats

Cited by 4 publications

References 27 publications

Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways

Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways

Effects of Limb Remote Postconditioning on Apoptosis and Long-Term Neurological Outcomes of Focal Cerebral Ischemia/Reperfusion Injury in Rats

Toward the Question of Ischemic Myocardial Dysfunction

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