Implication of mast cell degranulation in ischemic preconditioning‐induced prevention of cerebral injury

Rehni, Ashish K.; Bhateja, Pradeep; Singh, Nirmal; Jaggi, Amteshwar Singh

doi:10.1111/j.1472-8206.2008.00567.x

Cited by 32 publications

(30 citation statements)

References 29 publications

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“…Our own laboratory has documented protective eŠects of ischemic preconditioning in heart 10,11) and brain. 12,13) Moreover, pharmacological preconditioning, 14,15) remote preconditioning, 16,17) and ischemic post-conditioning 18) have been documented to produce tissue-protective eŠects. In the present investigation, stress as an insult was analogous to the ischemic insult and hence, accordingly short episodes of stress were employed before sustained restrain stress, analogous to protocols employed to investigate the protective eŠects of ischemic reconditioning.…”

Section: Discussionmentioning

confidence: 99%

“…Our own laboratory has documented the protective eŠects of ischemic preconditioning in heart 10,11) and brain. 12,13) This concept has been expanded to include pharmacological preconditioning, 14,15) remote preconditioning, 16,17) and ischemic post-conditioning. 18) The concept of ischemic and pharmacological preconditioning has been extrapolated to investigate the ameliorative role of stress preconditioning on stress-induced pathological changes and there have been reports suggesting the gastroprotective eŠects of stress preconditioning on cold, alcohol, restrain, and water immersion-induced gastric lesions in rats.…”

Section: Introductionmentioning

confidence: 99%

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Studies on Effect of Stress Preconditioning in Restrain Stress-induced Behavioral Alterations

2010

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Stress preconditioning has been documented to confer on gastroprotective eŠects on stress-induced gastric ulcerations. However, the eŠects of prior exposure of stress preconditioning episodes on stress-induced behavioral changes have not been explored yet. Therefore the present study was designed to investigate the ameliorative eŠects of stress preconditioning in immobilization stress-induced behavioral alterations in rats. The rats were subjected to restrain stress by placing in restrainer (5.5 cm in diameter and 18 cm in length) for 3.5 h. Stress preconditioning was induced by subjecting the rats to two cycles of restraint and restrain-free periods of 15 min each. Furthermore, a similar type of stress preconditioning was induced using diŠerent time cycles of 30 and 45 min. The extent and severity of the stress-induced behavioral alterations were assessed using diŠerent behavioral tests such as hole-board test, social interaction test, open eld test, and actophotometer. Restrain stress resulted in decrease in locomotor activity, frequency of head dips and rearing in hole board, line crossing and rearing in openˆeld, and decreased following and increased avoidance in social interaction test. Stress preconditioning with two cycles of 15, 30 or 45 min respectively, did not attenuate stress-induced behavioral changes to any extent. It may be concluded that stress preconditioning does not seem to confer any protective eŠect in modulating restrain stress-induced behavioral alterations.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Studies on Effect of Stress Preconditioning in Restrain Stress-induced Behavioral Alterations

2010

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“…21,23,24) Therefore, the assessment of cerebral infarct size using the triphenyltetrazolium chloride staining method and the quantitation of spatial memory and motor coordination using the elevated plus maze test and the rota-rod test respectively, were employed in order to assess the loss of brain structure and functions elicited by the ischemia-reperfusion injury as standardized earlier in our laboratory. [25][26][27][28] MATERIALS AND METHODS Swiss albino mice of either sex weighing 25Ϯ2 g, maintained on standard laboratory diet (Kisan Feeds Ltd., Mumbai, India) and having free access to tap water were employed in the present study. They were housed in the departmental animal house and were exposed to 12 h cycle of light and dark.…”

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“…Three such cycles of Ischemia and reperfusion were allowed immediately before (for acute preconditioning) and 24 h before (for delayed preconditioning) the bilateral carotid artery occlusion performed for 17 min. 25) Assessment of Cerebral Infarct Size At the end of 24 h of reperfusion after global cerebral ischemia, animals were sacrificed by spinal dislocation and the brain was removed. Brain samples were immediately sliced into uniform coronal sections of about 1 mm thickness.…”

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Possible Involvement of Ubiquitin Proteasome System and Other Proteases in Acute and Delayed Aspects of Ischemic Preconditioning of Brain in Mice

Rehni

Singh

Behl

et al. 2010

Biological & Pharmaceutical Bulletin

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Ischemic stroke is a syndrome characterized by rapid onset of neurological injury due to interruption of blood flow to the brain. 1) Although mortality from ischemic stroke has declined over the last decade but it still remains the third leading cause of death as only limited therapeutically strategies exist.2) Ischemic preconditioning is a potent protective strategy introduced by Murray and coworkers 3) for the ischemic myocardium which was later applied by Kitagawa et al. to the ischemic neuronal injury as well. 4)Multiple mediators have been shown to cause the protective effect produced by ischemic preconditioning of brain, including adenosine, acetylcholine, catecholamines, angiotensin II, bradykinin, endothelin and opioids.5-12) Ubiquitin-proteasome system and other proteases are few of the principal enzyme systems responsible for protein degradation and has been reported to be abundantly expressed in the various cell types of the central nervous system. 13,14) The addition of poly-ubiquitin chains to a protein results in its translocation to the proteasome, a large multi-subunit protease, which then results in its degradation. Recent in vitro reports have demonstrated the role of this ubiquitin-proteasome enzyme system as playing an essential role in rapid phase of ischemic preconditioning of cultured neurons. 15,16) Moreover, ubiquitin-proteasome system activation is one of the important mechanisms regulating the cell death pathways in ischemic neurons.13) And given the fact that a sub-threshold activation of various cell death pathways has been reported to contribute towards the biochemical progression of the phenomenon of preconditioning.17) Further, a recent experimental report has indicated the involvement of ubiquitin-proteasome system activation in mediating the cardioprotective effect of different phases of ischemic preconditioning of myocardial cells.18) Z-Leu-Leu-Phe-Chinese hamster ovary (CHO) is a cell permeable proteasome inhibitor acting on the ubiquitin proteasome enzyme system. 19) Therefore, the present study has been designed to evaluate the possible effect of Z-Leu-Leu-Phe-CHO (2 mg/kg, intraperitoneally (i.p.)), a selective inhibitor of ubiquitin proteasome system and other proteases, 19) on acute and delayed aspects of ischemic preconditioning induced protection of the mouse brain.Various research groups have reported that an episode of severe ischemia followed by reperfusion induces a marked cell death in the rodent brain. [20][21][22] This cell damage has been shown to be of diffused nature and is spread throughout the brain including the hippocampus and the motor cortex. 21,23,24) Therefore, the assessment of cerebral infarct size using the triphenyltetrazolium chloride staining method and the quantitation of spatial memory and motor coordination using the elevated plus maze test and the rota-rod test respectively, were employed in order to assess the loss of brain structure and functions elicited by the ischemia-reperfusion injury as standardized earlier in our laboratory. [25][26]...

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Mast cells: an expanding pathophysiological role from allergy to other disorders

Anand

Singh

Jaggi

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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The mast cells are multi-effector cells with wide distribution in the different body parts and traditionally their role has been well-defined in the development of IgE-mediated hypersensitivity reactions including bronchial asthma. Due to the availability of genetically modified mast cell-deficient mice, the broadened pathophysiological role of mast cells in diverse diseases has been revealed. Mast cells exert different physiological and pathophysiological roles by secreting their granular contents, including vasoactive amines, cytokines and chemokines, and various proteases, including tryptase and chymase. Furthermore, mast cells also synthesize plasma membrane-derived lipid mediators, including prostaglandins and leukotrienes, to produce diverse biological actions. The present review discusses the pathophysiological role of mast cells in different diseases, including atherosclerosis, pulmonary hypertension, ischemia-reperfusion injury, male infertility, autoimmune disorders such as rheumatoid arthritis and multiple sclerosis, bladder pain syndrome (interstitial cystitis), anxiety, Alzheimer's disease, nociception, obesity and diabetes mellitus.

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Implication of mast cell degranulation in ischemic preconditioning‐induced prevention of cerebral injury

Cited by 32 publications

References 29 publications

Studies on Effect of Stress Preconditioning in Restrain Stress-induced Behavioral Alterations

Studies on Effect of Stress Preconditioning in Restrain Stress-induced Behavioral Alterations

Possible Involvement of Ubiquitin Proteasome System and Other Proteases in Acute and Delayed Aspects of Ischemic Preconditioning of Brain in Mice

Mast cells: an expanding pathophysiological role from allergy to other disorders

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