MOLECULAR APOPTOSIS MECHANISMS WITH UNDERLYING EXPERIMENTAL ACUTE LUNG INJURY
Наукові журнали Тернопільського державного медичного університету імені І.Я.Горбачевського
Переглянути архів Інформація| Поле | Співвідношення | |
| Title |
MOLECULAR APOPTOSIS MECHANISMS WITH UNDERLYING EXPERIMENTAL ACUTE LUNG INJURY
MOLECULAR APOPTOSIS MECHANISMS WITH UNDERLYING EXPERIMENTAL ACUTE LUNG INJURY |
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| Creator |
Marushchak, M. I.
Klishch, I. M. Bondarenko, Yu. I. Mazur, L. P. |
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| Description |
Background. Current data suggest systemic autoimmune activation in the pathogenesis of bronchopulmonarydiseases. The imbalance in the system of pro- and anti-inflammatory cytokines is very important inimmunopathogenesis.Objective. The aim of our research was to determine the caspase-3 rate in the dynamics of experimentalacute lung injury and to study the relationship between their level and the number of cells carrying membranebinding TNF receptor type 1 to define the main mechanisms of cell death.Results. The analysis of the results of caspase-3 rate in lung homogenate showed that this cysteine proteinasewas uniformly increasing in all experimental groups during simulating of ALI induced by administration ofhydrochloric acid (p<0.001). When comparing the results of caspase course of apoptosis it was defined that,despite the progressive increase in caspase-3 rate in lung homogenate, cysteine proteinase rate in plasma didnot change.The receptor mechanism of apoptosis was studied by establishing correlation relationships with the numberof cells carrying membrane binding TNF type 1 (TNF-R1) receptor. A strong positive correlation relationshipbetween the number of neutrophils with TNF-R1 and caspase-3 rate in lungs of all research groups wasdetermined.Conclusions. The implementation of neutrophils death by apoptosis is caused by change of activity ofcaspase cascade effector components, such as caspase-3, in cases of ALI induced by intratracheal administrationof hydrochloric acid. One of the potential mechanisms responsible for the activation of caspase course is excessivegeneration of active forms of oxygen and increase in the number of neutrophils carrying membrane binding TNFreceptor type 1.KEY WORDS: caspase-3, tumour necrosis factor alpha receptor 1, acute lung injury
Background. Current data suggest systemic autoimmune activation in the pathogenesis of bronchopulmonarydiseases. The imbalance in the system of pro- and anti-inflammatory cytokines is very important inimmunopathogenesis.Objective. The aim of our research was to determine the caspase-3 rate in the dynamics of experimentalacute lung injury and to study the relationship between their level and the number of cells carrying membranebinding TNF receptor type 1 to define the main mechanisms of cell death.Results. The analysis of the results of caspase-3 rate in lung homogenate showed that this cysteine proteinasewas uniformly increasing in all experimental groups during simulating of ALI induced by administration ofhydrochloric acid (p<0.001). When comparing the results of caspase course of apoptosis it was defined that,despite the progressive increase in caspase-3 rate in lung homogenate, cysteine proteinase rate in plasma didnot change.The receptor mechanism of apoptosis was studied by establishing correlation relationships with the numberof cells carrying membrane binding TNF type 1 (TNF-R1) receptor. A strong positive correlation relationshipbetween the number of neutrophils with TNF-R1 and caspase-3 rate in lungs of all research groups wasdetermined.Conclusions. The implementation of neutrophils death by apoptosis is caused by change of activity ofcaspase cascade effector components, such as caspase-3, in cases of ALI induced by intratracheal administrationof hydrochloric acid. One of the potential mechanisms responsible for the activation of caspase course is excessivegeneration of active forms of oxygen and increase in the number of neutrophils carrying membrane binding TNFreceptor type 1.KEY WORDS: caspase-3, tumour necrosis factor alpha receptor 1, acute lung injury |
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| Publisher |
Ternopil State Medical University
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| Contributor |
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| Date |
2016-05-12
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| Type |
info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion — |
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| Format |
application/pdf
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| Identifier |
http://ojs.tdmu.edu.ua/index.php/ijmr/article/view/6382
10.11603/ijmmr.2413-6077.2016.1.6382 |
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| Source |
International Journal of Medicine and Medical Research; № 1 (2016)
International Jornal of Medicine and Medical Research; № 1 (2016) International Journal of Medicine and Medical Research; № 1 (2016) 2414-9985 2413-6077 10.11603/ijmmr.2413-6077.2015.2 |
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| Language |
ukr
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| Relation |
http://ojs.tdmu.edu.ua/index.php/ijmr/article/view/6382/5843
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| Rights |
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