Involvement of src-kinase activation in ischemic preconditioning induced protection of mouse brain

Rehni, Ashish K.; Singh, Thakur Gurjeet; Kakkar, Tarun; Arora, Sandeep

doi:10.1016/j.lfs.2011.02.024

Cited by 20 publications

(11 citation statements)

References 35 publications

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“…iPreCo just before global cerebral ischemia followed by reperfusion significantly found to attenuated ischemia?reperfusion induced increase in cerebral infarct size, increased motor incoordination, and impairment of memory. Pretreatment of SU‐6656 (2 mg/kg, ip) as well as PP1 (0.1 mg/kg, ip) prevented iPreCo induced decrease in cerebral infarct size and improvement in motor coordination and memory . In another study by Patel et al.…”

Section: Pharmacological Implications Of Src Kinasesmentioning

confidence: 91%

“…iPreCo just before global cerebral ischemia followed by reperfusion significantly found to attenuated ischemia-reperfusion induced increase in cerebral infarct size, increased motor incoordination, and impairment of memory. Pretreatment of SU-6656 (2 mg/kg, ip) as well as PP1 (0.1 mg/kg, ip) prevented iPreCo induced decrease in cerebral infarct size and improvement in motor coordination and memory [98]. In another study by Patel et al [99], mouse heart was isolated, and after mounting on Lengendorff assembly, ischemia was induced by 30 min of occlusion, followed by reperfusion for 2 h; PC in these heart with isoflurane resulted in decreased infarct size and produced elevation of phosphorylated Src and Cav-1, whereas treatment of mice with the Src inhibitor PP2 decreased Src and Cav-1 phosphorylation in the heart and reduced infarct size [99].…”

Section: Ischemic Preconditioningmentioning

confidence: 96%

“…A recent report by Rehni et al. demonstrates neuroprotective effect of Src kinase in iPreCo which can be abolished by pretreatment with Src kinase inhibitors SU6656 and PP1. In this study, 13 global cerebral ischemia of 17 min followed by reperfusion of 24 h produced a significant increase in cerebral infarct size, increase in motor incoordination, and impairment of memory.…”

Section: Pharmacological Implications Of Src Kinasesmentioning

confidence: 97%

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Pharmacology of Src family kinases and therapeutic implications of their modulators

Kumar

Jaggi

Singh

2015

Fundamemntal Clinical Pharma

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Src family kinases (SFKs), the largest family of nonreceptor tyrosine kinases, include 10 members. Src was the first gene product discovered to have intrinsic protein tyrosine kinase activity. Src is widely expressed in many cell types and can have different locations within a cell; the subcellular location of Src can affect its function. Src can associate with cellular membranes, such as the plasma membrane, the perinuclear membrane, and the endosomal membrane. SFKs actions on mammalian cells are pleiotropic and include effect on cell morphology, adhesion, migration, invasion, proliferation, differentiation, and survival. SFKs at one end have been documented to play some important physiological functions; on the other end, they have been described in the pathophysiology of some disorders. In this review article, an exhaustive attempt has been made to unearth pharmacology of SFKs and therapeutic implications of SFKs modulators.

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Section: Pharmacological Implications Of Src Kinasesmentioning

confidence: 91%

Section: Ischemic Preconditioningmentioning

confidence: 96%

Section: Pharmacological Implications Of Src Kinasesmentioning

confidence: 97%

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Pharmacology of Src family kinases and therapeutic implications of their modulators

Kumar

Jaggi

Singh

2015

Fundamemntal Clinical Pharma

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“…Therefore, in cardiac surgery, strict pH control is imperative. 71 Ouabain activates Src-kinase 55 indicating potential application of this endogenous hormone in neuroprotection. 68 Remote ischemic preconditioning is a powerful innate mechanism of multiorgan protection that can be induced by transient occlusion of blood flow to a limb with a blood-pressure cuff.…”

Section: Ouabain Mimics the Effects Of Hypoxie Lieninmentioning

confidence: 99%

Ouabain—The Key to Cardioprotection?

Fuerstenwerth¹

2014

American Journal of Therapeutics

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Based on a wealth of mechanistic evidence supported by the fact that ouabain mimics the spleen-liver effect in this article, the hypothesis is established that the endogenous hormone ouabain not only mimics the effects of ischemic preconditioning but also may be an ideal drug for the prevention of ischemic diseases. Moreover, it is argued that the spleen-liver effect may represent a general protective mechanism for the protection of organisms against oxygen deficiency. Investigating the spleen-liver mechanism offers a new approach to decipher the secrets of ischemic conditioning. Preconditioning represents a basic mechanism to protect a wide variety of cells against stressful stimuli such as ischemia. The ability to undergo preconditioning is almost ubiquitous in tissues and is highly conserved across species. Reinvestigation of the "spleen-liver mechanism" will allow the study of metabolic inhibitors and hormone mimics that all could help to transform ischemic preconditioning into a cure of the epidemic ischemic heart disease. Ouabain mimics the effects of the spleen factor. Cardioprotection induced by ouabain is due to the activation of pathways that are also activated in ischemic preconditioning. Just like ischemic preconditioning, ouabain activates the reperfusion injury salvage kinase pathway. Activation of nuclear factor kappa B and other transcription factors contribute to the long lasting effects of ouabain. The endogenous hormone ouabain just like preconditioning offers multiorgan protection based on innate mechanisms, which warrants clinical investigation. Clinical studies with ouabain that correspond to current standards are warranted.

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“…IPC is an adaptive technique whereby brief episodes of ischemia with intermittent reperfusion given immediately before the onset of ischemia and reperfusion protect the tissue against infarction resulting from a subsequent longer ischemic insult . IPC has been well reported to reduce myocardial injury and cerebral injury , improve postischemic recovery, and preserve vascular endothelial function . Although preconditioning has been successful in various clinical settings, inability to predict the onset of ischemia resulted in the discovery of a new concept of ischemic postconditioning (iPoCo) , whereby brief repetitive cycles of ischemia with intermittent reperfusion that follows after ischemia just prior to institution of prolonged reperfusion elicit tissue protection .…”

Section: Introductionmentioning

confidence: 99%

Evidence for the role of histaminergic pathways in neuroprotective mechanism of ischemic postconditioning in mice

Kaur

Kumar

Jaggi

et al. 2017

Fundamemntal Clinical Pharma

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The present study has been designed to investigate the possible role of histaminergic pathway in neuroprotective mechanism of ischemic postconditioning (iPoCo). Bilateral carotid artery occlusion (BCAO) for 12 min followed by reperfusion for 24 h was employed to produce I/R-induced cerebral injury in National Institutes of Health mice mice. iPoCo involving three episodes of carotid artery occlusion and reperfusion of 10 sec each was instituted immediately after BCAO just before prolonged reperfusion. Cerebral infarct size was measured using triphenyltetrazolium chloride staining. Memory was evaluated using Morris water maze test. Rotarod test, inclined beam-walking test, and neurological severity score (NSS) were performed to assess motor incoordination and sensorimotor abilities. Brain acetylcholine esterase (AChE) activity, brain myeloperoxidase (MPO) activity, brain thiobarbituric acid-reactive species (TBARS), and glutathione level (GSH) were also estimated. BCAO produced a significant rise in cerebral infarct size and NSS along with impairment of memory and motor coordination and biochemical alteration (↑AChE, ↑MPO ↓GSH, and ↑TBARS). iPoCo attenuated the deleterious effect of BCAO on infarct size, memory, NSS, motor coordination, and biochemical markers. Pretreatment of carnosine (a histamine [HA] precursor) potentiated the neuroprotective effects of iPoCo, whereas pretreatment of ketotifen (HA H1 receptor blocker and mast cell stabilizer) abolished the protective effects of iPoCo as well as that of carnosine on iPoCo. It may be concluded that neuroprotective effect of iPoCo probably involves activation of histaminergic pathways.

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Involvement of src-kinase activation in ischemic preconditioning induced protection of mouse brain

Cited by 20 publications

References 35 publications

Pharmacology of Src family kinases and therapeutic implications of their modulators

Pharmacology of Src family kinases and therapeutic implications of their modulators

Ouabain—The Key to Cardioprotection?

Evidence for the role of histaminergic pathways in neuroprotective mechanism of ischemic postconditioning in mice

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